Valerius-pub-2017.bib

%% Created using Papers on Mon, 11 Dec 2017. %% http://papersapp.com/papers/

@article{Naiman:2017cja, author = {Naiman, Natalie and Fujioka, Kaoru and Fujino, Mari and Valerius, M Todd and Potter, S Steven and McMahon, Andrew P and Kobayashi, Akio}, title = {{Repression of Interstitial Identity in Nephron Progenitor Cells by Pax2 Establishes the Nephron-Interstitium Boundary during Kidney Development.}}, journal = {Developmental cell}, year = {2017}, volume = {41}, number = {4}, pages = {349--365.e3}, month = may, affiliation = {Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.}, doi = {10.1016/j.devcel.2017.04.022}, pmid = {28535371}, pmcid = {PMC5532731}, language = {English}, rating = {0}, date-added = {2017-12-11T16:59:45GMT}, date-modified = {2017-12-11T17:01:36GMT}, abstract = {The kidney contains the functional units, the nephrons, surrounded by the renal interstitium. Previously we discovered that, once Six2-expressing nephron progenitor cells and Foxd1-expressing renal interstitial progenitor cells form at the onset of kidney development, descendant cells from these populations contribute exclusively to the main body of nephrons and renal interstitial tissues, respectively, indicating a lineage boundary between the nephron and renal interstitial compartments. Currently it is unclear how lineages are regulated during kidney organogenesis. We demonstrate that nephron progenitor cells lacking Pax2 fail to differentiate into nephron cells but can switch fates into renal interstitium-like~cell types. These data suggest that Pax2 function~maintains nephron progenitor cells by repressing a renal interstitial cell program. Thus, the lineage boundary between the nephron and renal interstitial compartments is maintained by the Pax2 activity in~nephron progenitor cells during kidney organogenesis.}, url = {http://linkinghub.elsevier.com/retrieve/pii/S1534580717303489}, uri = {\url{papers3://publication/doi/10.1016/j.devcel.2017.04.022}} }

@article{Oxburgh:2017fxa, author = {Oxburgh, Leif and Carroll, Thomas J and Cleaver, Ondine and Gossett, Daniel R and Hoshizaki, Deborah K and Hubbell, Jeffrey A and Humphreys, Benjamin D and Jain, Sanjay and Jensen, Jan and Kaplan, David L and Kesselman, Carl and Ketchum, Christian J and Little, Melissa H and McMahon, Andrew P and Shankland, Stuart J and Spence, Jason R and Valerius, M Todd and Wertheim, Jason A and Wessely, Oliver and Zheng, Ying and Drummond, Iain A}, title = {{(Re)Building a Kidney.}}, journal = {Journal of the American Society of Nephrology}, year = {2017}, volume = {28}, number = {5}, pages = {1370--1378}, month = may, affiliation = {Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, Maine; oxburl@mmc.org idrummond@mgh.harvard.edu.}, doi = {10.1681/ASN.2016101077}, pmid = {28096308}, pmcid = {PMC5407737}, language = {English}, rating = {0}, date-added = {2017-12-11T16:59:45GMT}, date-modified = {2017-12-11T17:01:36GMT}, abstract = {(Re)Building a Kidney is a National Institute of Diabetes and Digestive and Kidney Diseases-led consortium to optimize approaches for the isolation, expansion, and differentiation of appropriate kidney cell types and the integration of these cells into complex structures that replicate human kidney function. The ultimate goals of the consortium are two-fold: to develop and implement strategies for in vitro engineering of replacement kidney tissue, and to devise strategies to stimulate regeneration of nephrons in situ to restore failing kidney function. Projects within the consortium will answer fundamental questions regarding human gene expression in the developing kidney, essential signaling crosstalk between distinct cell types of the developing kidney, how to derive the many cell types of the kidney through directed differentiation of human pluripotent stem cells, which bioengineering or scaffolding strategies have the most potential for kidney tissue formation, and basic parameters of the regenerative response to injury. As these projects progress, the consortium will incorporate systematic investigations in physiologic function of in vitro and in vivo differentiated kidney tissue, strategies for engraftment in experimental animals, and development of therapeutic approaches to activate innate reparative responses.}, url = {http://www.jasn.org/lookup/doi/10.1681/ASN.2016101077}, uri = {\url{papers3://publication/doi/10.1681/ASN.2016101077}} }

@article{Togel:2017jfa, author = {T{\"o}gel, Florian and Valerius, M Todd and Freedman, Benjamin S and Iatrino, Rossella and Grinstein, Mor and Bonventre, Joseph V}, title = {{Repair after nephron ablation reveals limitations of neonatal neonephrogenesis.}}, journal = {JCI insight}, year = {2017}, volume = {2}, number = {2}, pages = {e88848}, month = jan, affiliation = {Renal Division, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.}, doi = {10.1172/jci.insight.88848}, pmid = {28138555}, pmcid = {PMC5256143}, language = {English}, rating = {0}, date-added = {2017-12-11T16:59:45GMT}, date-modified = {2017-12-11T17:01:36GMT}, abstract = {The neonatal mouse kidney retains nephron progenitor cells in a nephrogenic zone for 3 days after birth. We evaluated whether de novo nephrogenesis can be induced postnatally beyond 3 days. Given the long-term implications of nephron number for kidney health, it would be useful to enhance nephrogenesis in the neonate. We induced nephron reduction by cryoinjury with or without contralateral nephrectomy during the neonatal period or after 1 week of age. There was no detectable compensatory de novo nephrogenesis, as determined by glomerular counting and lineage tracing. Contralateral nephrectomy resulted in additional adaptive healing, with little or no fibrosis, but did not also stimulate de novo nephrogenesis. In contrast, injury initiated at 1 week of age led to healing with fibrosis. Thus, despite the presence of progenitor cells and ongoing nephron maturation in the newborn mouse kidney, de novo nephrogenesis is not inducible by acute nephron reduction. This indicates that additional nephron progenitors cannot be recruited after birth despite partial renal ablation providing a reparative stimulus and suggests that nephron number in the mouse is predetermined at birth.}, url = {https://insight.jci.org/articles/view/88848}, uri = {\url{papers3://publication/doi/10.1172/jci.insight.88848}} }

@article{Valerius:2016ci, author = {Valerius, M Todd}, title = {{Human Kidney Organoids: Nephron Models of Development and Disease.}}, journal = {Transplantation}, year = {2016}, volume = {100}, number = {6}, pages = {1171--1172}, month = jun, affiliation = {1 Renal Division, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, MA; and Harvard Stem Cell Institute, Cambridge, MA.}, doi = {10.1097/TP.0000000000001233}, pmid = {27203586}, language = {English}, rating = {0}, date-added = {2017-12-11T16:59:45GMT}, date-modified = {2017-12-11T17:01:36GMT}, url = {http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00007890-201606000-00004}, uri = {\url{papers3://publication/doi/10.1097/TP.0000000000001233}} }

@article{Masuzaki:2016ixa, author = {Masuzaki, Ryota and Zhao, Sophia and Valerius, M Todd and Tsugawa, Daisuke and Oya, Yuki and Ray, Kevin C and Karp, Seth J}, title = {{SOCS2 Balances Metabolic and Restorative Requirements during Liver Regeneration.}}, journal = {The Journal of biological chemistry}, year = {2016}, volume = {291}, number = {7}, pages = {3346--3358}, month = feb, affiliation = {From the Transplant Center, Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232.}, doi = {10.1074/jbc.M115.703264}, pmid = {26703468}, pmcid = {PMC4751379}, language = {English}, rating = {0}, date-added = {2017-12-11T16:59:46GMT}, date-modified = {2017-12-11T17:01:36GMT}, abstract = {After significant injury, the liver must maintain homeostasis during the regenerative process. We hypothesized the existence of mechanisms to limit hepatocyte proliferation after injury to maintain metabolic and synthetic function. A screen for candidates revealed suppressor of cytokine signaling 2 (SOCS2), an inhibitor of growth hormone (GH) signaling, was strongly induced after partial hepatectomy. Using genetic deletion and administration of various factors we investigated the role of SOCS2 during liver regeneration. SOCS2 preserves liver function by restraining the first round of hepatocyte proliferation after partial hepatectomy by preventing increases in growth hormone receptor (GHR) via ubiquitination, suppressing GH pathway activity. At later times, SOCS2 enhances hepatocyte proliferation by modulating a decrease in serum insulin-like growth factor 1 (IGF-1) that allows GH release from the pituitary. SOCS2, therefore, plays a dual role in modulating the rate of hepatocyte proliferation. In particular, this is the first demonstration of an endogenous mechanism to limit hepatocyte proliferation after injury.}, url = {http://www.jbc.org/lookup/doi/10.1074/jbc.M115.703264}, uri = {\url{papers3://publication/doi/10.1074/jbc.M115.703264}} }

@article{Morizane:2015bq, author = {Morizane, Ryuji and Lam, Albert Q and Freedman, Benjamin S and Kishi, Seiji and Valerius, M Todd and Bonventre, Joseph V}, title = {{Nephron organoids derived from human pluripotent stem cells model kidney development and injury.}}, journal = {Nature biotechnology}, year = {2015}, volume = {33}, number = {11}, pages = {1193--1200}, month = nov, keywords = {{\&}organoids}, doi = {10.1038/nbt.3392}, pmid = {26458176}, pmcid = {PMC4747858}, language = {English}, read = {Yes}, rating = {0}, date-added = {2015-10-19T20:49:35GMT}, date-modified = {2017-09-06T18:02:42GMT}, abstract = {Kidney cells and tissues derived from human pluripotent stem cells (hPSCs) may enable organ regeneration, disease modeling and drug screening. We report an efficient, chemically defined protocol for differentiating hPSCs into multipotent nephron progenitor cells (NPCs) that can form nephron-like structures. By recapitulating metanephric kidney development in vitro, we generate SIX2+ SALL1+ WT1+ PAX2+ NPCs with 90% efficiency within 9 days of differentiation. The NPCs possess the developmental potential of their in vivo counterparts and form PAX8+ LHX1+ renal vesicles that self-organize into nephron structures. In both two- and three-dimensional culture, NPCs form kidney organoids containing epithelial nephron-like structures expressing markers of podocytes, proximal tubules, loops of Henle and distal tubules in an organized, continuous arrangement that resembles the nephron in vivo. We also show that this organoid culture system can be used to study mechanisms of human kidney development and toxicity.}, url = {http://www.nature.com/doifinder/10.1038/nbt.3392}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Files/30/30C5FD7E-9B28-4EF0-BC90-569C3745D7CE.pdf}, file = {{30C5FD7E-9B28-4EF0-BC90-569C3745D7CE.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Files/30/30C5FD7E-9B28-4EF0-BC90-569C3745D7CE.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1038/nbt.3392}} }

@article{Freedman:2015kua, author = {Freedman, Benjamin S and Brooks, Craig R and Lam, Albert Q and Fu, Hongxia and Morizane, Ryuji and Agrawal, Vishesh and Saad, Abdelaziz F and Li, Michelle K and Hughes, Michael R and Werff, Ryan Vander and Peters, Derek T and Lu, Junjie and Baccei, Anna and Siedlecki, Andrew M and Valerius, M Todd and Musunuru, Kiran and McNagny, Kelly M and Steinman, Theodore I and Zhou, Jing and Lerou, Paul H and Bonventre, Joseph V}, title = {{Modelling kidney disease with CRISPR-mutant kidney organoids derived from human pluripotent epiblast spheroids.}}, journal = {Nature communications}, year = {2015}, volume = {6}, pages = {8715}, month = oct, affiliation = {Division of Renal Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institutes of Medicine Suite 550, 4 Blackfan Circle, Boston, Massachusetts 02115, USA.}, doi = {10.1038/ncomms9715}, pmid = {26493500}, pmcid = {PMC4620584}, language = {English}, rating = {0}, date-added = {2017-12-11T17:00:17GMT}, date-modified = {2017-12-11T17:01:36GMT}, abstract = {Human-pluripotent-stem-cell-derived kidney cells (hPSC-KCs) have important potential for disease modelling and regeneration. Whether the hPSC-KCs can reconstitute tissue-specific phenotypes is currently unknown. Here we show that hPSC-KCs self-organize into kidney organoids that functionally recapitulate tissue-specific epithelial physiology, including disease phenotypes after genome editing. In three-dimensional cultures, epiblast-stage hPSCs form spheroids surrounding hollow, amniotic-like cavities. GSK3$\beta$ inhibition differentiates spheroids into segmented, nephron-like kidney organoids containing cell populations with characteristics of proximal tubules, podocytes and endothelium. Tubules accumulate dextran and methotrexate transport cargoes, and express kidney injury molecule-1 after nephrotoxic chemical injury. CRISPR/Cas9 knockout of podocalyxin causes junctional organization defects in podocyte-like cells. Knockout of the polycystic kidney disease genes PKD1 or PKD2 induces cyst formation from kidney tubules. All of these functional phenotypes are distinct from effects in epiblast spheroids, indicating that they are tissue specific. Our findings establish a reproducible, versatile three-dimensional framework for human epithelial disease modelling and regenerative medicine applications.}, url = {http://www.nature.com/doifinder/10.1038/ncomms9715}, uri = {\url{papers3://publication/doi/10.1038/ncomms9715}} }

@article{Baek:2015cm, author = {Baek, Jea-Hyun and Zeng, Rui and Weinmann-Menke, Julia and Valerius, M Todd and Wada, Yukihiro and Ajay, Amrendra K and Colonna, Marco and Kelley, Vicki R}, title = {{IL-34 mediates acute kidney injury and worsens subsequent chronic kidney disease.}}, journal = {The Journal of clinical investigation}, year = {2015}, volume = {125}, number = {8}, pages = {3198--3214}, month = aug, doi = {10.1172/JCI81166}, pmid = {26121749}, pmcid = {PMC4563757}, language = {English}, read = {Yes}, rating = {0}, date-added = {2015-10-19T21:59:21GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Macrophages (M{\o}) are integral in ischemia/reperfusion injury-incited (I/R-incited) acute kidney injury (AKI) that leads to fibrosis and chronic kidney disease (CKD). IL-34 and CSF-1 share a receptor (c-FMS), and both cytokines mediate M{\o} survival and proliferation but also have distinct features. CSF-1 is central to kidney repair and destruction. We tested the hypothesis that IL-34-dependent, M{\o}-mediated mechanisms promote persistent ischemia-incited AKI that worsens subsequent CKD. In renal I/R, the time-related magnitude of M{\o}-mediated AKI and subsequent CKD were markedly reduced in IL-34-deficient mice compared with controls. IL-34, c-FMS, and a second IL-34 receptor, protein-tyrosine phosphatase $\zeta$ (PTP-$\zeta$) were upregulated in the kidney after I/R. IL-34 was generated by tubular epithelial cells (TECs) and promoted M{\o}-mediated TEC destruction during AKI that worsened subsequent CKD via 2 distinct mechanisms: enhanced intrarenal M{\o} proliferation and elevated BM myeloid cell proliferation, which increases circulating monocytes that are drawn into the kidney by chemokines. CSF-1 expression in TECs did not compensate for IL-34 deficiency. In patients, kidney transplants subject to I/R expressed IL-34, c-FMS, and PTP-$\zeta$ in TECs during AKI that increased with advancing injury. Moreover, IL-34 expression increased, along with more enduring ischemia in donor kidneys. In conclusion, IL-34-dependent, M{\o}-mediated, CSF-1 nonredundant mechanisms promote persistent ischemia-incited AKI that worsens subsequent CKD.}, url = {http://www.jci.org/articles/view/81166}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Files/A9/A9FDAC26-7218-4979-9EB7-9D21B51C4EB5.pdf}, file = {{A9FDAC26-7218-4979-9EB7-9D21B51C4EB5.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Files/A9/A9FDAC26-7218-4979-9EB7-9D21B51C4EB5.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1172/JCI81166}} }

@article{Lindstrom:2014cz, author = {Lindstr{\"o}m, Nils O and Chang, C-Hong and Valerius, M Todd and Hohenstein, Peter and Davies, Jamie A}, title = {{Node retraction during patterning of the urinary collecting duct system.}}, journal = {Journal of anatomy}, year = {2015}, volume = {226}, number = {1}, pages = {13--21}, month = jan, affiliation = {Roslin Institute, University of Edinburgh, Easter Bush, UK.}, doi = {10.1111/joa.12239}, pmid = {25292187}, pmcid = {PMC4299504}, language = {English}, read = {Yes}, rating = {0}, date-added = {2014-10-11T22:04:28GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {This report presents a novel mechanism for remodelling a branched epithelial tree. The mouse renal collecting duct develops by growth and repeated branching of an initially unbranched ureteric bud: this mechanism initially produces an almost fractal form with young branches connected to the centre of the kidney via a sequence of nodes (branch points) distributed widely throughout the developing organ. The collecting ducts of a mature kidney have a different form: from the nephrons in the renal cortex, long, straight lengths of collecting duct run almost parallel to one another through the renal medulla, and open together to the renal pelvis. Here we present time-lapse studies of E11.5 kidneys growing in culture: after about 5~days, the collecting duct trees show evidence of 'node retraction', in which the node of a 'Y'-shaped branch moves downwards, shortening the stalk of the 'Y', lengthening its arms and narrowing their divergence angle so that the 'Y' becomes a 'V'. Computer simulation suggests that node retraction can transform a spread tree, like that of an early kidney, into one with long, almost-parallel medullary rays similar to those seen in a mature real kidney.}, url = {http://doi.wiley.com/10.1111/joa.12239}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2014/Lindstr%C3%B6m/J%20Anat%202014%20Lindstr%C3%B6m.pdf}, file = {{J Anat 2014 Lindström.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2014/Lindström/J Anat 2014 Lindström.pdf:application/pdf;J Anat 2014 Lindström.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2014/Lindström/J Anat 2014 Lindström.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1111/joa.12239}} }

@article{Lam:2014ba, author = {Lam, Albert Q and Freedman, Benjamin S and Morizane, Ryuji and Lerou, Paul H and Valerius, M Todd and Bonventre, Joseph V}, title = {{Rapid and efficient differentiation of human pluripotent stem cells into intermediate mesoderm that forms tubules expressing kidney proximal tubular markers.}}, journal = {Journal of the American Society of Nephrology}, year = {2014}, volume = {25}, number = {6}, pages = {1211--1225}, month = jun, affiliation = {Renal Division, Department of Medicine, and Harvard Stem Cell Institute, Cambridge, Massachusetts; and aqlam@partners.org.}, doi = {10.1681/ASN.2013080831}, pmid = {24357672}, pmcid = {PMC4033376}, language = {English}, read = {Yes}, rating = {0}, date-added = {2014-02-10T20:03:06GMT}, date-modified = {2016-12-06T21:44:37GMT}, abstract = {Human pluripotent stem cells (hPSCs) can generate a diversity of cell types, but few methods have been developed to derive cells of the kidney lineage. Here, we report a highly efficient system for differentiating human embryonic stem cells and induced pluripotent stem cells (referred to collectively as hPSCs) into cells expressing markers of the intermediate mesoderm (IM) that subsequently form tubule-like structures. Treatment of hPSCs with the glycogen synthase kinase-3$\beta$ inhibitor CHIR99021 induced BRACHYURY(+)MIXL1(+) mesendoderm differentiation with nearly 100% efficiency. In the absence of additional exogenous factors, CHIR99021-induced mesendodermal cells preferentially differentiated into cells expressing markers of lateral plate mesoderm with minimal IM differentiation. However, the sequential treatment of hPSCs with CHIR99021 followed by fibroblast growth factor-2 and retinoic acid generated PAX2(+)LHX1(+) cells with 70%-80% efficiency after 3 days of differentiation. Upon growth factor withdrawal, these PAX2(+)LHX1(+) cells gave rise to apically ciliated tubular structures that coexpressed the proximal tubule markers Lotus tetragonolobus lectin, N-cadherin, and kidney-specific protein and partially integrated into embryonic kidney explant cultures. With the addition of FGF9 and activin, PAX2(+)LHX1(+) cells specifically differentiated into cells expressing SIX2, SALL1, and WT1, markers of cap mesenchyme nephron progenitor cells. Our findings demonstrate the effective role of fibroblast growth factor signaling in inducing IM differentiation in hPSCs and establish the most rapid and efficient system whereby hPSCs can be differentiated into cells with features characteristic of kidney lineage cells.}, url = {http://www.jasn.org/cgi/doi/10.1681/ASN.2013080831}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2014/Lam/J%20Am%20Soc%20Nephrol%202014%20Lam.pdf}, file = {{J Am Soc Nephrol 2014 Lam.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2014/Lam/J Am Soc Nephrol 2014 Lam.pdf:application/pdf;J Am Soc Nephrol 2014 Lam.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2014/Lam/J Am Soc Nephrol 2014 Lam.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1681/ASN.2013080831}} }

@article{Park:2012hx, author = {Park, Joo-Seop and Ma, Wenxiu and O'Brien, Lori L and Chung, Eunah and Guo, Jin-Jin and Cheng, Jr-Gang and Valerius, M Todd and McMahon, Jill A and Wong, Wing Hung and McMahon, Andrew P}, title = {{Six2 and Wnt regulate self-renewal and commitment of nephron progenitors through shared gene regulatory networks.}}, journal = {Developmental cell}, year = {2012}, volume = {23}, number = {3}, pages = {637--651}, month = sep, affiliation = {Division of Pediatric Urology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. joo-seop.park@cchmc.org}, doi = {10.1016/j.devcel.2012.07.008}, pmid = {22902740}, pmcid = {PMC3892952}, language = {English}, read = {Yes}, rating = {0}, date-added = {2012-09-05T15:52:04GMT}, date-modified = {2017-08-15T15:21:42GMT}, abstract = {A balance between Six2-dependent self-renewal and canonical Wnt signaling-directed commitment regulates mammalian nephrogenesis. Intersectional studies using chromatin immunoprecipitation and transcriptional profiling identified direct target genes shared by each pathway within nephron progenitors. Wnt4 and Fgf8 are essential for progenitor commitment; cis-regulatory modules flanking each gene are cobound by Six2 and $\beta$-catenin and are dependent on conserved Lef/Tcf binding sites for activity. In~vitro and in~vivo analyses suggest that Six2 and~Lef/Tcf factors form a regulatory complex that promotes progenitor maintenance while entry of $\beta$-catenin into this complex promotes nephrogenesis. Alternative transcriptional responses associated with Six2 and $\beta$-catenin cobinding events occur through non-Lef/Tcf DNA binding mechanisms, highlighting the regulatory complexity downstream of Wnt signaling in the developing mammalian kidney.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22902740&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2012/Park/Dev%20Cell%202012%20Park.pdf}, file = {{Dev Cell 2012 Park.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Park/Dev Cell 2012 Park.pdf:application/pdf;Dev Cell 2012 Park.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Park/Dev Cell 2012 Park.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.devcel.2012.07.008}} }

@article{Yu:2012ik, author = {Yu, Jing and Valerius, M Todd and Duah, Mary and Staser, Karl and Hansard, Jennifer K and Guo, Jin-Jin and McMahon, Jill and Vaughan, Joe and Faria, Diane and Georgas, Kylie and Rumballe, Bree and Ren, Qun and Krautzberger, A Michaela and Junker, Jan P and Thiagarajan, Rathi D and Machanick, Philip and Gray, Paul A and van Oudenaarden, Alexander and Rowitch, David H and Stiles, Charles D and Ma, Qiufu and Grimmond, Sean M and Bailey, Timothy L and Little, Melissa H and McMahon, Andrew P}, title = {{Identification of molecular compartments and genetic circuitry in the developing mammalian kidney.}}, journal = {Development (Cambridge, England)}, year = {2012}, volume = {139}, number = {10}, pages = {1863--1873}, month = may, annote = {Fig. S1. Raw data of single molecule fluorescent in situ hybridization. (A-D) Raw data (A,B) and filtered data (C,D) for single molecule FISH experiments. (A,B) Raw data for Foxi1-Alexa594 and Gsdmc-Cy5. Individual diffraction-limited dots corresponding to single mRNA molecules can be clearly distinguished in the data. (C,D) Filtered data (Laplacian of Gaussian) for automated dot detection, as previously described (Raj et al., 2008).}, affiliation = {Department of Stem Cell and Regenerative Biology, Department of Molecular and Cellular Biology, Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.}, doi = {10.1242/dev.074005}, pmid = {22510988}, pmcid = {PMC3328182}, language = {English}, read = {Yes}, rating = {5}, date-added = {2012-05-08T16:02:55GMT}, date-modified = {2016-12-06T21:43:56GMT}, abstract = {Lengthy developmental programs generate cell diversity within an organotypic framework, enabling the later physiological actions of each organ system. Cell identity, cell diversity and cell function are determined by cell type-specific transcriptional programs; consequently, transcriptional regulatory factors are useful markers of emerging cellular complexity, and their expression patterns provide insights into the regulatory mechanisms at play. We performed a comprehensive genome-scale in situ expression screen of 921 transcriptional regulators in the developing mammalian urogenital system. Focusing on the kidney, analysis of regional-specific expression patterns identified novel markers and cell types associated with development and patterning of the urinary system. Furthermore, promoter analysis of synexpressed genes predicts transcriptional control mechanisms that regulate cell differentiation. The annotated informational resource (www.gudmap.org) will facilitate functional analysis of the mammalian kidney and provides useful information for the generation of novel genetic tools to manipulate emerging cell populations.}, url = {http://dev.biologists.org/cgi/doi/10.1242/dev.074005}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2012/Yu/Development%202012%20Yu.pdf}, file = {{Development 2012 Yu.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Yu/Development 2012 Yu.pdf:application/pdf;Development 2012 Yu.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Yu/Development 2012 Yu.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1242/dev.074005}} }

@article{Balasubramanian:2012gi, author = {Balasubramanian, Savithri and Jansen, Marcel and Valerius, M Todd and Humphreys, Benjamin D and Strom, Terry B}, title = {{Orphan nuclear receptor Nur77 promotes acute kidney injury and renal epithelial apoptosis.}}, journal = {Journal of the American Society of Nephrology}, year = {2012}, volume = {23}, number = {4}, pages = {674--686}, month = apr, affiliation = {Department of Medicine, The Transplant Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.}, doi = {10.1681/ASN.2011070646}, pmid = {22343121}, pmcid = {PMC3312507}, language = {English}, rating = {0}, date-added = {2012-02-24T21:47:50GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Nur77 and its family members Nurr1 and Nor-1 are inducible orphan nuclear receptors that orchestrate cellular responses to diverse extracellular signals. In epithelia, Nur77 can act as a potent proapoptotic molecule in response to cellular stress, suggesting a possible role for this nuclear receptor in the tissue response to injury. Here, we found that Nur77 promotes epithelial cell apoptosis after AKI. Injury of proximal tubular epithelial cells rapidly and strongly induced Nur77, Nor-1, and Nurr1 both in vitro and in vivo. After renal ischemia-reperfusion, Nurr77-deficient mice exhibited less apoptosis of tubular epithelial cells and better renal function than wild-type mice. Nur77-mediated renal injury involved a conformational change of Bcl2 and an increase in the protein levels of proapoptotic Bcl-xS. Ligand-activated retinoic acid receptors repressed Nur77 induction and function. Pretreatment of wild-type mice with retinoic acid before renal ischemia-reperfusion blunted the induction of Nur77, conferred protection of renal function, attenuated renal histologic injury, and reduced the expression of epithelial-derived proinflammatory cytokines. Retinoic acid also inhibited hypoxia-mediated induction of proinflammatory cytokines in cultured renal epithelial cells. Results obtained from proximal tubule cultures derived from Nur77-deficient mice suggested that the inhibition of Nur77 expression mediated the renoprotective effects of retinoic acid. In summary, Nur77 promotes epithelial apoptosis after ischemia-reperfusion injury, and retinoic acid-mediated inhibition of Nur77 expression is a promising therapeutic strategy for the prevention of AKI.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22343121&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2012/Balasubramanian/J%20Am%20Soc%20Nephrol%202012%20Balasubramanian.pdf}, file = {{J Am Soc Nephrol 2012 Balasubramanian.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Balasubramanian/J Am Soc Nephrol 2012 Balasubramanian.pdf:application/pdf;J Am Soc Nephrol 2012 Balasubramanian.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Balasubramanian/J Am Soc Nephrol 2012 Balasubramanian.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1681/ASN.2011070646}} }

@article{Valerius:2012ef, author = {Valerius, M Todd}, title = {{Bowman's $\beta$-catenin.}}, journal = {Journal of the American Society of Nephrology}, year = {2012}, volume = {23}, number = {1}, pages = {3--4}, month = jan, doi = {10.1681/ASN.2011111106}, pmid = {22158436}, language = {English}, read = {Yes}, rating = {0}, date-added = {2012-01-09T15:56:46GMT}, date-modified = {2016-09-29T21:02:08GMT}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22158436&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2012/Valerius/J%20Am%20Soc%20Nephrol%202012%20Valerius.pdf}, file = {{J Am Soc Nephrol 2012 Valerius.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Valerius/J Am Soc Nephrol 2012 Valerius.pdf:application/pdf;J Am Soc Nephrol 2012 Valerius.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Valerius/J Am Soc Nephrol 2012 Valerius.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1681/ASN.2011111106}} }

@article{Wiese:2012ej, author = {Wiese, Carrie B and Ireland, Sara and Fleming, Nicole L and Yu, Jing and Valerius, M Todd and Georgas, Kylie and Chiu, Han Sheng and Brennan, Jane and Armstrong, Jane and Little, Melissa H and McMahon, Andrew P and Southard-Smith, E Michelle}, title = {{A genome-wide screen to identify transcription factors expressed in pelvic Ganglia of the lower urinary tract.}}, journal = {Frontiers in neuroscience}, year = {2012}, volume = {6}, pages = {130}, affiliation = {Division of Genetic Medicine, Department of Medicine, Vanderbilt University School of Medicine Nashville, TN, USA.}, doi = {10.3389/fnins.2012.00130}, pmid = {22988430}, pmcid = {PMC3439845}, language = {English}, read = {Yes}, rating = {0}, date-added = {2012-12-02T00:29:36GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Relative positions of neurons within mature murine pelvic ganglia based on expression of neurotransmitters have been described. However the spatial organization of developing innervation in the murine urogenital tract (UGT) and the gene networks that regulate specification and maturation of neurons within the pelvic ganglia of the lower urinary tract (LUT) are unknown. We used whole-mount immunohistochemistry and histochemical stains to localize neural elements in 15.5 days post coitus (dpc) fetal mice. To identify potential regulatory factors expressed in pelvic ganglia, we surveyed expression patterns for known or probable transcription factors (TF) annotated in the mouse genome by screening a whole-mount in situ hybridization library of fetal UGTs. Of the 155 genes detected in pelvic ganglia, 88 encode TFs based on the presence of predicted DNA-binding domains. Neural crest (NC)-derived progenitors within the LUT were labeled by Sox10, a well-known regulator of NC development. Genes identified were categorized based on patterns of restricted expression in pelvic ganglia, pelvic ganglia and urethral epithelium, or pelvic ganglia and urethral mesenchyme. Gene expression patterns and the distribution of Sox10+, Phox2b+, Hu+, and PGP9.5+ cells within developing ganglia suggest previously unrecognized regional segregation of Sox10+ progenitors and differentiating neurons in early development of pelvic ganglia. Reverse transcription-PCR of pelvic ganglia RNA from fetal and post-natal stages demonstrated that multiple TFs maintain post-natal expression, although Pax3 is extinguished before weaning. Our analysis identifies multiple potential regulatory genes including TFs that may participate in segregation of discrete lineages within pelvic ganglia. The genes identified here are attractive candidate disease genes that may now be further investigated for their roles in malformation syndromes or in LUT dysfunction.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22988430&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2012/Wiese/Front%20Neurosci%202012%20Wiese.pdf}, file = {{Front Neurosci 2012 Wiese.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Wiese/Front Neurosci 2012 Wiese.pdf:application/pdf;Front Neurosci 2012 Wiese.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2012/Wiese/Front Neurosci 2012 Wiese.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.3389/fnins.2012.00130}} }

@article{Boyle:2011bz, author = {Boyle, S C and Boyle, Scott C and Kim, Mijin and Kim, M and Valerius, M Todd and Valerius, M T and McMahon, Andrew P and McMahon, A P and Kopan, Raphael and Kopan, R}, title = {{Notch pathway activation can replace the requirement for Wnt4 and Wnt9b in mesenchymal-to-epithelial transition of nephron stem cells}}, journal = {Development (Cambridge, England)}, year = {2011}, volume = {138}, number = {19}, pages = {4245--4254}, month = sep, annote = { {\textbullet} Supplemental Figure S1 - Fig. S1. N1ICD-expressing CMM cells only make PT and immature POD in vivo. Segment-specific markers were examined in E15.5 kidneys from RosaN1ICD and Six2CreRosaN1ICD animals. (A-F) NI1CD kidneys express Wt1, indicating podocyte commitment (C-F) but not more terminal markers Mafb (A,B) and synaptopodin (E,F) or proper glomerular morphology (C-F). (G-P) Among segment specific markers, PT (Scl34a1) can be detected but not markers of the LOH (I-L), DT (M,N) or CMT (O,P). {\textbullet} Supplemental Figure S2 - Fig. S2. 3T3-Wnt4 cells induce tubulogenesis in isolated mesenchyme and rescue tubular formation in Wnt4{\&}lt;b{\&}gt;{\textminus}{\&}lt;/b{\&}gt;/{\&}lt;b{\&}gt;{\textminus} kidneys. (A,B) MM was mechanically isolated from E11.5 kidney explants and grown of either 3T3-lacZ (A) or 3T3-Wnt4 cells (B). Robust differentiation was observed only in Wnt4-treated cultures (B). (C,D) E12.5 Wnt4{\textminus}/{\textminus} kidneys were isolated and grown in the same manner. Wnt4 cells rescue differentiation in Wnt4{\textminus}/{\textminus} kidneys (D, arrows). {\textbullet} Supplemental Figure S3 - Fig. S3. Heat map of mRNA levels of Notch receptors and ligands in selected cellular compartments. Figure generated using microarray data deposited in the GUDMAP database http://www.gudmap.org by the Potter group using sorted cells from indicated compartments for expression profiling. Data retrieved 5/25/11. High levels of Notch1, Notch4 and Dll4 and the absence of Notch2 in the endothelium demonstrate the fidelity of the analysis. Notch1, Notch2, Dll1 and Jag1 are all strongly upregulated in the RV, corresponding to known protein expression patterns and consistent with what we believe the site of action for Notch in nephron development based on mutant phenotypes. With the exception of Notch2, these genes are not expressed in the CMM until it is undergoing its final round of differentiation (P4), when it takes on the characteristics of the RV, demonstrating that Notch signaling is not active in the CMM.}, doi = {10.1242/dev.070433}, pmid = {21852398}, pmcid = {PMC3171224}, language = {English}, rating = {0}, date-added = {2011-10-17T18:59:07GMT}, date-modified = {2016-09-29T21:02:08GMT}, url = {http://dev.biologists.org/cgi/doi/10.1242/dev.070433}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2011/Boyle/Development%202011%20Boyle.pdf}, file = {{Development 2011 Boyle.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2011/Boyle/Development 2011 Boyle.pdf:application/pdf;Development 2011 Boyle.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2011/Boyle/Development 2011 Boyle.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1242/dev.070433}} }

@article{Balasubramanian:2011cb, author = {Balasubramanian, Savithri and Kota, Satya K and Valerius, M Todd}, title = {{The rejection barrier to induced pluripotent stem cells.}}, journal = {Journal of the American Society of Nephrology : JASN}, year = {2011}, volume = {22}, number = {9}, pages = {1583--1586}, month = sep, doi = {10.1681/ASN.2011070707}, pmid = {21836145}, language = {English}, rating = {0}, date-added = {2011-08-17T16:57:58GMT}, date-modified = {2016-09-29T21:02:08GMT}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21836145&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2011/Balasubramanian/J%20Am%20Soc%20Nephrol%202011%20Balasubramanian.pdf}, file = {{J Am Soc Nephrol 2011 Balasubramanian.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2011/Balasubramanian/J Am Soc Nephrol 2011 Balasubramanian.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1681/ASN.2011070707}} }

@article{Nagalakshmi:2011gx, author = {Nagalakshmi, Vidya K and Ren, Qun and Pugh, Margaret M and Valerius, M Todd and McMahon, Andrew P and Yu, Jing}, title = {{Dicer regulates the development of nephrogenic and ureteric compartments in the mammalian kidney.}}, journal = {Kidney international}, year = {2011}, volume = {79}, number = {3}, pages = {317--330}, month = feb, affiliation = {Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.}, doi = {10.1038/ki.2010.385}, pmid = {20944551}, pmcid = {PMC3214622}, language = {English}, rating = {0}, date-added = {2011-06-20T12:46:26GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {MicroRNAs (miRNAs) are a large and growing class of small, non-coding, regulatory RNAs that control gene expression predominantly at the post-transcriptional level. The production of most functional miRNAs depends on the enzymatic activity of Dicer, an RNase III class enzyme. To address the potential action of Dicer-dependent miRNAs in mammalian kidney development, we conditionally ablated Dicer function within cells of nephron lineage and the ureteric bud-derived collecting duct system. Six2Cre-mediated removal of Dicer activity from the progenitors of the nephron epithelium led to elevated apoptosis and premature termination of nephrogenesis. Thus, Dicer action is important for maintaining the viability of this critical self-renewing progenitor pool and, consequently, development of a normal nephron complement. HoxB7Cre-mediated removal of Dicer function from the ureteric bud epithelium led to the development of renal cysts. This was preceded by excessive cell proliferation and apoptosis, and accompanied by disrupted ciliogenesis within the ureteric bud epithelium. Dicer removal also disrupted branching morphogenesis with the phenotype correlating with downregulation of Wnt11 and c-Ret expression at ureteric tips. Thus Dicer, and by inference Dicer-dependent miRNA activity, have distinct regulatory roles within different components of the developing mouse kidney. Furthermore, an understanding of miRNA action may provide new insights into the etiology and pathogenesis of renal cyst-based kidney disease.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20944551&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2011/Nagalakshmi/Kidney%20Int%202011%20Nagalakshmi.pdf}, file = {{Kidney Int 2011 Nagalakshmi.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2011/Nagalakshmi/Kidney Int 2011 Nagalakshmi.pdf:application/pdf;Kidney Int 2011 Nagalakshmi.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2011/Nagalakshmi/Kidney Int 2011 Nagalakshmi.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1038/ki.2010.385}} }

@article{Humphreys:2010da, author = {Humphreys, Benjamin D and Lin, Shuei-Liong and Kobayashi, Akio and Hudson, Thomas E and Nowlin, Brian T and Bonventre, Joseph V and Valerius, M Todd and McMahon, Andrew P and Duffield, Jeremy S}, title = {{Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis.}}, journal = {The American journal of pathology}, year = {2010}, volume = {176}, number = {1}, pages = {85--97}, month = jan, affiliation = {Renal Division, Department of Medicine, Brigham {\&} Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.}, doi = {10.2353/ajpath.2010.090517}, pmid = {20008127}, pmcid = {PMC2797872}, language = {English}, read = {Yes}, rating = {0}, date-added = {2010-02-23T19:13:02GMT}, date-modified = {2017-06-05T20:09:50GMT}, abstract = {Understanding the origin of myofibroblasts in kidney is of great interest because these cells are responsible for scar formation in fibrotic kidney disease. Recent studies suggest epithelial cells are an important source of myofibroblasts through a process described as the epithelial-to-mesenchymal transition; however, confirmatory studies in vivo are lacking. To quantitatively assess the contribution of renal epithelial cells to myofibroblasts, we used Cre/Lox techniques to genetically label and fate map renal epithelia in models of kidney fibrosis. Genetically labeled primary proximal epithelial cells cultured in vitro from these mice readily induce markers of myofibroblasts after transforming growth factor beta(1) treatment. However, using either red fluorescent protein or beta-galactosidase as fate markers, we found no evidence that epithelial cells migrate outside of the tubular basement membrane and differentiate into interstitial myofibroblasts in vivo. Thus, although renal epithelial cells can acquire mesenchymal markers in vitro, they do not directly contribute to interstitial myofibroblast cells in vivo. Lineage analysis shows that during nephrogenesis, FoxD1-positive((+)) mesenchymal cells give rise to adult CD73(+), platelet derived growth factor receptor beta(+), smooth muscle actin-negative interstitial pericytes, and these FoxD1-derivative interstitial cells expand and differentiate into smooth muscle actin(+) myofibroblasts during fibrosis, accounting for a large majority of myofibroblasts. These data indicate that therapeutic strategies directly targeting pericyte differentiation in vivo may productively impact fibrotic kidney disease.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20008127&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2010/Humphreys/Am%20J%20Pathol%202010%20Humphreys.pdf}, file = {{Am J Pathol 2010 Humphreys.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2010/Humphreys/Am J Pathol 2010 Humphreys.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.2353/ajpath.2010.090517}} }

@article{Georgas:2009bv, author = {Georgas, Kylie and Rumballe, Bree and Valerius, M Todd and Chiu, Han Sheng and Thiagarajan, Rathi D and Lesieur, Emmanuelle and Aronow, Bruce J and Brunskill, Eric W and Combes, Alexander N and Tang, Dave and Taylor, Darrin and Grimmond, Sean M and Potter, S Steven and McMahon, Andrew P and Little, Melissa H}, title = {{Analysis of early nephron patterning reveals a role for distal RV proliferation in fusion to the ureteric tip via a cap mesenchyme-derived connecting segment}}, journal = {Developmental biology}, year = {2009}, volume = {332}, number = {2}, pages = {273--286}, month = aug, doi = {10.1016/j.ydbio.2009.05.578}, pmid = {19501082}, pmcid = {NIHMS123047}, language = {English}, read = {Yes}, rating = {0}, date-added = {2009-10-13T20:43:59GMT}, date-modified = {2017-08-14T20:01:53GMT}, url = {http://linkinghub.elsevier.com/retrieve/pii/S0012160609009105}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2009/Georgas/Dev.%20Biol.%202009%20Georgas.pdf}, file = {{Dev. Biol. 2009 Georgas.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2009/Georgas/Dev. Biol. 2009 Georgas.pdf:application/pdf;Dev. Biol. 2009 Georgas.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2009/Georgas/Dev. Biol. 2009 Georgas.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.ydbio.2009.05.578}} }

@article{Brunskill:2008gc, author = {Brunskill, Eric W and Aronow, Bruce J and Georgas, Kylie and Rumballe, Bree and Valerius, M Todd and Aronow, Jeremy and Kaimal, Vivek and Jegga, Anil G and Yu, Jing and Grimmond, Sean and McMahon, Andrew P and Patterson, Larry T and Little, Melissa H and Potter, S Steven}, title = {{Atlas of gene expression in the developing kidney at microanatomic resolution.}}, journal = {Developmental cell}, year = {2008}, volume = {15}, number = {5}, pages = {781--791}, month = nov, affiliation = {Division of Developmental Biology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.}, doi = {10.1016/j.devcel.2008.09.007}, pmid = {19000842}, pmcid = {PMC2653061}, language = {English}, read = {Yes}, rating = {0}, date-added = {2009-01-25T21:41:29GMT}, date-modified = {2016-12-06T21:44:37GMT}, abstract = {Kidney development is based on differential cell-type-specific expression of a vast number of genes. While multiple critical genes and pathways have been elucidated, a genome-wide analysis of gene expression within individual cellular and anatomic structures is lacking. Accomplishing this could provide significant new insights into fundamental developmental mechanisms such as mesenchymal-epithelial transition, inductive signaling, branching morphogenesis, and segmentation. We describe here a comprehensive gene expression atlas of the developing mouse kidney based on the isolation of each major compartment by either laser capture microdissection or fluorescence-activated cell sorting, followed by microarray profiling. The resulting data agree with known expression patterns and additional in situ hybridizations. This kidney atlas allows a comprehensive analysis of the progression of gene expression states during nephrogenesis, as well as discovery of potential growth factor-receptor interactions. In addition, the results provide deeper insight into the genetic regulatory mechanisms of kidney development.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19000842&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2008/Brunskill/Dev%20Cell%202008%20Brunskill.pdf}, file = {{Dev Cell 2008 Brunskill.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2008/Brunskill/Dev Cell 2008 Brunskill.pdf:application/pdf;Dev Cell 2008 Brunskill.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2008/Brunskill/Dev Cell 2008 Brunskill.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.devcel.2008.09.007}} }

@article{Kobayashi:2008fh, author = {Kobayashi, Akio and Valerius, M Todd and Mugford, Joshua W and Carroll, Thomas J and Self, Michelle and Oliver, Guillermo and McMahon, Andrew P}, title = {{Six2 defines and regulates a multipotent self-renewing nephron progenitor population throughout mammalian kidney development.}}, journal = {Cell Stem Cell}, year = {2008}, volume = {3}, number = {2}, pages = {169--181}, month = aug, affiliation = {Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.}, doi = {10.1016/j.stem.2008.05.020}, pmid = {18682239}, pmcid = {PMC2561900}, language = {English}, read = {Yes}, rating = {0}, date-added = {2008-08-15T14:07:18GMT}, date-modified = {2016-12-06T21:44:37GMT}, abstract = {Nephrons, the basic functional units of the kidney, are generated repetitively during kidney organogenesis from a mesenchymal progenitor population. Which cells within this pool give rise to nephrons and how multiple nephron lineages form during this protracted developmental process are unclear. We demonstrate that the Six2-expressing cap mesenchyme represents a multipotent nephron progenitor population. Six2-expressing cells give rise to all cell types of the main body of the nephron during all stages of nephrogenesis. Pulse labeling of Six2-expressing nephron progenitors at the onset of kidney development suggests that the Six2-expressing population is maintained by self-renewal. Clonal analysis indicates that at least some Six2-expressing cells are multipotent, contributing to multiple domains of the nephron. Furthermore, Six2 functions cell autonomously to maintain a progenitor cell status, as cap mesenchyme cells lacking Six2 activity contribute to ectopic nephron tubules, a mechanism dependent on a Wnt9b inductive signal. Taken together, our observations suggest that Six2 activity cell-autonomously regulates a multipotent nephron progenitor population.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18682239&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2008/Kobayashi/Cell%20Stem%20Cell%202008%20Kobayashi.pdf}, file = {{Cell Stem Cell 2008 Kobayashi.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2008/Kobayashi/Cell Stem Cell 2008 Kobayashi.pdf:application/pdf;Cell Stem Cell 2008 Kobayashi.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2008/Kobayashi/Cell Stem Cell 2008 Kobayashi.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.stem.2008.05.020}} }

@article{Valerius:2008ks, author = {Valerius, M Todd and McMahon, Andrew P}, title = {{Transcriptional profiling of Wnt4 mutant mouse kidneys identifies genes expressed during nephron formation.}}, journal = {Gene expression patterns : GEP}, year = {2008}, volume = {8}, number = {5}, pages = {297--306}, month = may, affiliation = {Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.}, doi = {10.1016/j.gep.2008.02.001}, pmid = {18346943}, pmcid = {PMC2435058}, language = {English}, read = {Yes}, rating = {0}, date-added = {2008-07-04T21:18:51GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {The mature nephron forms from a simple epithelial vesicle into an elaborate structure with distinct regions of specialized physiological function. The molecular components driving the process of nephron development are not well understood. To identify genes that may be informative in this process we conducted a transcriptional profiling screen using Wnt4 mutant kidneys. In Wnt4-/- homozygous mice, condensates and pretubular aggregates are induced, however, epithelial renal vesicles fail to form and subsequent tubulogenesis is blocked. A transcriptional profile comparison between wildtype and Wnt4-/- mutant kidneys at E14.5 was performed using Affymetrix oligonucleotide microarrays to identify nephron-expressed genes. This approach identified 236 genes with expression levels >1.8-fold higher in wildtype versus mutant kidneys, amongst these were a number of known nephron component markers confirming the validity of the screen. These results were further detailed by wholemount in situ hybridization (WISH) of E15.5 urogenital systems (UGS). We annotated the spatial expression pattern of these genes into eight categories of expression. Genes expressed in renal vesicle and their derivatives, structures absent in the mutant, accounted for the largest number of the observed expression patterns. A number of additional genes in areas not directly overlapping the Wnt4 expression domain were also identified including the cap mesenchyme, the collecting duct, and the cortical interstitium. This study provides a useful compendium of molecular markers for the study of nephrogenesis.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18346943&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2008/Valerius/Gene%20Expr%20Patterns%202008%20Valerius.pdf}, file = {{Gene Expr Patterns 2008 Valerius.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2008/Valerius/Gene Expr Patterns 2008 Valerius.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.gep.2008.02.001}} }

@article{Humphreys:2008dz, author = {Humphreys, Benjamin D and Valerius, M Todd and Kobayashi, Akio and Mugford, Joshua W and Soeung, Savuth and Duffield, Jeremy S and McMahon, Andrew P and Bonventre, Joseph V}, title = {{Intrinsic epithelial cells repair the kidney after injury.}}, journal = {Cell Stem Cell}, year = {2008}, volume = {2}, number = {3}, pages = {284--291}, month = mar, affiliation = {Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Institutes of Medicine, Room 550, 4 Blackfan Circle, Boston, MA 02115, USA. bhumphreys@partners.org}, doi = {10.1016/j.stem.2008.01.014}, pmid = {18371453}, language = {English}, read = {Yes}, rating = {0}, date-added = {2008-03-30T02:38:48GMT}, date-modified = {2017-06-05T20:09:50GMT}, abstract = {Understanding the mechanisms of nephron repair is critical for the design of new therapeutic approaches to treat kidney disease. The kidney can repair after even a severe insult, but whether adult stem or progenitor cells contribute to epithelial renewal after injury and the cellular origin of regenerating cells remain controversial. Using genetic fate-mapping techniques, we generated transgenic mice in which 94%-95% of tubular epithelial cells, but no interstitial cells, were labeled with either beta-galactosidase (lacZ) or red fluorescent protein (RFP). Two days after ischemia-reperfusion injury (IRI), 50.5% of outer medullary epithelial cells coexpress Ki67 and RFP, indicating that differentiated epithelial cells that survived injury undergo proliferative expansion. After repair was complete, 66.9% of epithelial cells had incorporated BrdU, compared to only 3.5% of cells in the uninjured kidney. Despite this extensive cell proliferation, no dilution of either cell-fate marker was observed after repair. These results indicate that regeneration by surviving tubular epithelial cells is the predominant mechanism of repair after ischemic tubular injury in the adult mammalian kidney.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18371453&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2008/Humphreys/Cell%20Stem%20Cell%202008%20Humphreys.pdf}, file = {{Cell Stem Cell 2008 Humphreys.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2008/Humphreys/Cell Stem Cell 2008 Humphreys.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.stem.2008.01.014}} }

@article{Little:2007gp, author = {Little, Melissa H and Brennan, Jane and Georgas, Kylie and Davies, Jamie A and Davidson, Duncan R and Baldock, Richard A and Beverdam, Annemiek and Bertram, John F and Capel, Blanche and Chiu, Han Sheng and Clements, Dave and Cullen-McEwen, Luise and Fleming, Jean and Gilbert, Thierry and Herzlinger, Doris and Houghton, Derek and Kaufman, Matt H and Kleymenova, Elena and Koopman, Peter A and Lewis, Alfor G and McMahon, Andrew P and Mendelsohn, Cathy L and Mitchell, Eleanor K and Rumballe, Bree A and Sweeney, Derina E and Valerius, M Todd and Yamada, Gen and Yang, Yiya and Yu, Jing}, title = {{A high-resolution anatomical ontology of the developing murine genitourinary tract.}}, journal = {Gene expression patterns : GEP}, year = {2007}, volume = {7}, number = {6}, pages = {680--699}, month = jun, affiliation = {Institute for Molecular Bioscience, University of Queensland, Brisbane 4072, Australia. M.Little@imb.uq.edu.au}, keywords = {{\&}gudmap, {\&}kidney, {\&}ontology, {\&}reprint}, doi = {10.1016/j.modgep.2007.03.002}, pmid = {17452023}, pmcid = {PMC2117077}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:42:00GMT}, date-modified = {2017-03-03T20:11:04GMT}, abstract = {Cataloguing gene expression during development of the genitourinary tract will increase our understanding not only of this process but also of congenital defects and disease affecting this organ system. We have developed a high-resolution ontology with which to describe the subcompartments of the developing murine genitourinary tract. This ontology incorporates what can be defined histologically and begins to encompass other structures and cell types already identified at the molecular level. The ontology is being used to annotate in situ hybridisation data generated as part of the Genitourinary Development Molecular Anatomy Project (GUDMAP), a publicly available data resource on gene and protein expression during genitourinary development. The GUDMAP ontology encompasses Theiler stage (TS) 17-27 of development as well as the sexually mature adult. It has been written as a partonomic, text-based, hierarchical ontology that, for the embryological stages, has been developed as a high-resolution expansion of the existing Edinburgh Mouse Atlas Project (EMAP) ontology. It also includes group terms for well-characterised structural and/or functional units comprising several sub-structures, such as the nephron and juxtaglomerular complex. Each term has been assigned a unique identification number. Synonyms have been used to improve the success of query searching and maintain wherever possible existing EMAP terms relating to this organ system. We describe here the principles and structure of the ontology and provide representative diagrammatic, histological, and whole mount and section RNA in situ hybridisation images to clarify the terms used within the ontology. Visual examples of how terms appear in different specimen types are also provided.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=17452023&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2007/Little/Gene%20Expr%20Patterns%202007%20Little.pdf}, file = {{Gene Expr Patterns 2007 Little.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2007/Little/Gene Expr Patterns 2007 Little.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.modgep.2007.03.002}} }

@article{Park:2007hn, author = {Park, J S and Park, Joo-Seop and Valerius, M Todd and Valerius, M T and McMahon, Andrew P and McMahon, A P}, title = {{Wnt/~-catenin signaling regulates nephron induction during mouse kidney development}}, journal = {Development (Cambridge, England)}, year = {2007}, volume = {134}, number = {13}, pages = {2533--2539}, month = may, doi = {10.1242/dev.006155}, pmid = {17537789}, language = {English}, read = {Yes}, rating = {0}, date-added = {2010-06-16T19:38:42GMT}, date-modified = {2016-09-29T21:02:08GMT}, url = {http://dev.biologists.org/cgi/doi/10.1242/dev.006155}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2007/Park/Development%202007%20Park.pdf}, file = {{Development 2007 Park.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2007/Park/Development 2007 Park.pdf:application/pdf;Development 2007 Park.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2007/Park/Development 2007 Park.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1242/dev.006155}} }

@article{Cheng:2007jx, author = {Cheng, H T and Cheng, Hui-Teng and Kim, Mijin and Kim, M and Valerius, M Todd and Valerius, M T and Surendran, Kameswaran and Surendran, K and Schuster-Gossler, Karin and Schuster-Gossler, K and Gossler, A and Gossler, Achim and McMahon, A P and McMahon, Andrew P and Kopan, Raphael and Kopan, R}, title = {{Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron}}, journal = {Development (Cambridge, England)}, year = {2007}, volume = {134}, number = {4}, pages = {801--811}, month = jan, doi = {10.1242/dev.02773}, pmid = {17229764}, pmcid = {PMC2613851}, language = {English}, read = {Yes}, rating = {5}, date-added = {2007-03-27T14:08:36GMT}, date-modified = {2016-09-29T21:02:08GMT}, url = {http://dev.biologists.org/cgi/doi/10.1242/dev.02773}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2007/Cheng/Development%202007%20Cheng.pdf}, file = {{Development 2007 Cheng.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2007/Cheng/Development 2007 Cheng.pdf:application/pdf;Development 2007 Cheng.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2007/Cheng/Development 2007 Cheng.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1242/dev.02773}} }

@article{Gray:2004fo, author = {Gray, Paul A and Fu, Hui and Luo, Ping and Zhao, Qing and Yu, Jing and Ferrari, Annette and Tenzen, Toyoaki and Yuk, Dong-In and Tsung, Eric F and Cai, Zhaohui and Alberta, John A and Cheng, Le-Ping and Liu, Yang and Stenman, Jan M and Valerius, M Todd and Billings, Nathan and Kim, Haesun A and Greenberg, Michael E and McMahon, Andrew P and Rowitch, David H and Stiles, Charles D and Ma, Qiufu}, title = {{Mouse brain organization revealed through direct genome-scale TF expression analysis.}}, journal = {Science (New York, NY)}, year = {2004}, volume = {306}, number = {5705}, pages = {2255--2257}, month = dec, affiliation = {Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.}, doi = {10.1126/science.1104935}, pmid = {15618518}, language = {English}, rating = {0}, date-added = {2012-02-03T23:05:18GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {In the developing brain, transcription factors (TFs) direct the formation of a diverse array of neurons and glia. We identifed 1445 putative TFs in the mouse genome. We used in situ hybridization to map the expression of over 1000 of these TFs and TF-coregulator genes in the brains of developing mice. We found that 349 of these genes showed restricted expression patterns that were adequate to describe the anatomical organization of the brain. We provide a comprehensive inventory of murine TFs and their expression patterns in a searchable brain atlas database.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=15618518&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2004/Gray/Science%202004%20Gray.pdf}, file = {{Science 2004 Gray.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2004/Gray/Science 2004 Gray.pdf:application/pdf;Science 2004 Gray.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2004/Gray/Science 2004 Gray.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1126/science.1104935}} }

@article{Yu:2004ey, author = {Yu, Jing and McMahon, Andrew P and Valerius, M Todd}, title = {{Recent genetic studies of mouse kidney development.}}, journal = {Current opinion in genetics {\&} development}, year = {2004}, volume = {14}, number = {5}, pages = {550--557}, month = oct, affiliation = {Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA.}, keywords = {{\&}kidney}, doi = {10.1016/j.gde.2004.07.009}, pmid = {15380247}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:48:05GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Recent functional studies in mouse further illustrate the importance of the epithelial-mesenchymal interaction between the ureteric bud epithelium and the metanephric mesenchyme in kidney formation. Genetic ablation of Gdf11, Six1, Slit2/Robo2 reveal a role of these genes in regulating the outgrowth of a single ureteric bud from the Wolffian duct. Studies of Wnt11 and Fras1/Grip1, all expressed in the ureteric bud, show a role for these genes in regulating events in the adjacent metanephric mesenchyme. Furthermore, various approaches were used to address the function of Pod1, Pbx1, the Notch pathway and Brn1 in nephron formation.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=15380247&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2004/Yu/Curr%20Opin%20Genet%20Dev%202004%20Yu.pdf}, file = {{Curr Opin Genet Dev 2004 Yu.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2004/Yu/Curr Opin Genet Dev 2004 Yu.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1016/j.gde.2004.07.009}} }

@article{Valerius:2002cr, author = {Valerius, M Todd and Patterson, Larry T and Feng, Yuxin and Potter, S Steven}, title = {{Hoxa 11 is upstream of Integrin alpha8 expression in the developing kidney.}}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, year = {2002}, volume = {99}, number = {12}, pages = {8090--8095}, month = jun, affiliation = {Division of Developmental Biology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.}, keywords = {{\&}kidney}, doi = {10.1073/pnas.122229199}, pmid = {12060755}, pmcid = {PMC123025}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:49:00GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Mutation of the functionally redundant Hoxa 11/Hoxd 11 genes gives absent or rudimentary kidneys resulting from a dramatic reduction of the growth and branching of the ureteric bud. To understand better the molecular mechanisms of Hoxa 11/Hoxd 11 function in kidney development, it is necessary to identify the downstream target genes regulated by their encoded transcription factors. To this end, we conducted a screen for Hoxa 11-responsive genes in two kidney cell lines. HEK293 cells, which usually do not express Hoxa 11, were modified to allow inducible Hoxa 11 expression. The mK10 cells, derived specifically for this study from Hoxa 11/Hoxd 11 double-mutant mice, were also modified to give cell populations with and without Hoxa 11 expression. Differential display, Gene Discovery Arrays, and Affymetrix genechip probe arrays were used to screen for genes up- or down-regulated by Hoxa 11. Nine genes, PDGF A, Cathepsin L, annexin A1, Mm.112139, Est2 repressor factor, NrCAM, ZNF192, integrin-associated protein, and GCM1, showed reproducible 3-fold or smaller changes in gene expression in response to Hoxa 11. One gene, the Integrin alpha8, was up-regulated approximately 20-fold after Hoxa 11 expression. The Integrin alpha8 gene is expressed together with Hoxa 11 in metanephric mesenchyme cells, and mutation of Integrin alpha8 gives a bud-branching morphogenesis defect very similar to that observed in Hoxa 11/Hoxd 11 mutant mice. In situ hybridizations showed a dramatic regional reduction in Integrin alpha8 expression in the developing kidneys of Hoxa 11/Hoxd 11 mutant mice. This work suggests that the Integrin alpha8 gene may be a major effector of Hoxa 11/Hoxd 11 function in the developing kidney.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=12060755&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2002/Valerius/Proc%20Natl%20Acad%20Sci%20USA%202002%20Valerius.pdf}, file = {{Proc Natl Acad Sci USA 2002 Valerius.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2002/Valerius/Proc Natl Acad Sci USA 2002 Valerius.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1073/pnas.122229199}} }

@article{Valerius:2002td, author = {Valerius, M Todd and Patterson, Larry T and Witte, David P and Potter, S Steven}, title = {{Microarray analysis of novel cell lines representing two stages of metanephric mesenchyme differentiation.}}, journal = {Mechanisms of development}, year = {2002}, volume = {112}, number = {1-2}, pages = {219--232}, month = mar, affiliation = {Division of Developmental Biology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.}, keywords = {{\&}kidney, {\&}microarray}, pmid = {11850199}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:49:43GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Clonal cell lines representing different developmental stages of the metanephric mesenchyme were made from transgenic mice with the Simian Virus 40 T-antigen (SV40 Tag) gene driven by the Hoxa 11 promoter. The resulting mK3 cell line represented early metanephric mesenchyme, prior to induction by the ureteric bud. These cells showed a spindle-shaped, fibroblast morphology. They expressed genes characteristic of early mesenchyme, including Hoxa 11, Hoxd 11, collagen I, and vimentin. Moreover, the mK3 cells displayed early metanephric mesenchyme biological function. In organ co-culture experiments they were able to induce growth and branching of the ureteric bud. Another cell line, mK4, represented later, induced metanephric mesenchyme undergoing epithelial conversion. These cells were more polygonal, or epithelial in shape, and expressed genes diagnostic of late mesenchyme, including Pax-2, Pax-8, Wnt-4, Cadherin-6, Collagen IV, and LFB3. To better define the gene expression patterns of kidney metanephric mesenchyme cells at these two stages of development, RNAs from the mK3 and mK4 cells were hybridized to Affymetrix GeneChip probe arrays. Over 4000 expressed genes were identified and thereby implicated in kidney formation. Comparison of the mK3 and mK4 gene expression profiles revealed 121 genes showing greater than a ten-fold difference in expression level. Several are known to be expressed during metanephric mesenchyme differentiation, but most had not been previously associated with this process. In situ hybridizations were used to confirm that selected novel genes were expressed in the developing kidney.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=11850199&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/2002/Valerius/Mech%20Dev%202002%20Valerius.pdf}, file = {{Mech Dev 2002 Valerius.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/2002/Valerius/Mech Dev 2002 Valerius.pdf:application/pdf}}, uri = {\url{papers3://publication/uuid/C8E6B1DA-0187-455D-B26F-449C3E31523F}} }

@article{Potter:2002ux, author = {Potter, S S and Valerius, M T and Brunskill, E W}, title = {{Using progenitor cells and gene chips to define genetic pathways.}}, journal = {Methods in molecular biology (Clifton, NJ)}, year = {2002}, volume = {185}, pages = {269--284}, affiliation = {Division of Developmental Biology, Children's Hospital Medical Center, Cincinnati, OH, USA.}, pmid = {11768995}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:50:20GMT}, date-modified = {2016-09-29T21:02:08GMT}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=11768995&retmode=ref&cmd=prlinks}, uri = {\url{papers3://publication/uuid/FD8FA916-ED70-4032-BAA0-DCE5D13D48A1}} }

@article{Branford:1997uf, author = {Branford, W W and Zhao, G Q and Valerius, M T and Weinstein, M and Birkenmeier, E H and Rowe, L B and Potter, S S}, title = {{Spx1, a novel X-linked homeobox gene expressed during spermatogenesis.}}, journal = {Mechanisms of development}, year = {1997}, volume = {65}, number = {1-2}, pages = {87--98}, month = jul, affiliation = {Children's Hospital Research Foundation, Developmental Biology, Cincinnati, OH 45229, USA.}, pmid = {9256347}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:51:14GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Spx1, a novel mouse homeobox gene, encodes a homeodomain characteristic of the paired-like class of homeobox genes and has been mapped to the distal end of the X chromosome. Northern blot hybridization of adult tissues detected high levels of a single Spx1 transcript in the testis. Further analysis by in situ hybridization revealed predominant Spx1 expression within the spermatogonia/preleptotene spermatocytes and round spermatids of spermatogenic stages IV-VII. These expression data suggest SPX1 may play a role in the regulation of spermatogenesis.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=9256347&retmode=ref&cmd=prlinks}, uri = {\url{papers3://publication/uuid/C444B485-1F35-4F1A-8628-6450419DEBFB}} }

@article{Haynes:1996vz, author = {Haynes, T L and Thomas, M B and Dusing, M R and Valerius, M T and Potter, S S and Wiginton, D A}, title = {{An enhancer LEF-1/TCF-1 site is essential for insertion site-independent transgene expression in thymus.}}, journal = {Nucleic acids research}, year = {1996}, volume = {24}, number = {24}, pages = {5034--5044}, month = dec, affiliation = {Department of Pediatrics, University of Cincinnati, OH 45229, USA.}, pmid = {9016677}, pmcid = {PMC146351}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:51:14GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {Transcriptional activation of eukaryotic genes involves assembly of specific multiprotein complexes on the promoters and enhancers of the genes. Recently, it has been proposed that the role of some of the proteins in the complex may be architectural, involving DNA bending, orchestration of protein-protein interaction and modulation of nucleosome structure. This role has been proposed for the HMG proteins LEF-1 and TCF-1. We examined the role of a LEF-1/TCF-1 binding site in the human adenosine deaminase (ADA) thymic enhancer. Mutational analysis demonstrated that a functional LEF-1/TCF-1 binding site is not required for enhancer-mediated transcriptional activation in transient transfection studies, but is essential for enhancer function in the in vivo chromatin context of transgenic mice. Mutation of the LEF-1/TCF-1 site destroyed the ability of the ADA enhancer/locus control region to specify high level, insertion site-independent transgene expression in thymus. DNase I and DpnII accessibility experiments indicated dramatic changes in the chromatin organization of the ADA enhancer in transgenic mice with a mutated LEF-1/TCF-1 site. This supports the hypothesis that factors binding the LEF-1/TCF-1 site play an architectural role during the in vivo activation of the ADA enhancer, possibly involving chromatin modification.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=9016677&retmode=ref&cmd=prlinks}, uri = {\url{papers3://publication/uuid/F7F664BB-15D9-43B2-B651-62986BC27ACC}} }

@article{Li:1996wx, author = {Li, H and Zeitler, P S and Valerius, M T and Small, K and Potter, S S}, title = {{Gsh-1, an orphan Hox gene, is required for normal pituitary development.}}, journal = {The EMBO journal}, year = {1996}, volume = {15}, number = {4}, pages = {714--724}, month = feb, affiliation = {Department of Pediatrics, University of Cincinnati College of Medicine, OH 45229-3039, USA.}, pmid = {8631293}, pmcid = {PMC450270}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:51:14GMT}, date-modified = {2016-09-29T21:02:08GMT}, abstract = {The anterior pituitary regulates the function of multiple organ systems as well as body growth, and in turn is controlled by peptides released by the hypothalamus. We find that mutation of the Gsh-1 homeobox gene results in pleiotropic effects on pituitary development and function. Homozygous mutants exhibit extreme dwarfism, sexual infantilism and significant perinatal mortality. The mutant pituitary is small in size and hypocellular, with severely reduced numbers of growth hormone- and prolactin-producing cells. Moreover, the pituitary content of a subset of pituitary hormones, including growth hormone, prolactin and luteinizing hormone, is significantly decreased. The hypothalamus, although morphologically normal, is also perturbed in mutants. The gsh-1 gene is shown to be essential for growth hormone-releasing hormone (GHRH) gene expression in the arcuate nucleus of the hypothalamus. Further, sequence and electrophoretic mobility shift data suggest the Gsh-1 and GHRH genes as potential targets regulated by the Gsh-1-encoded protein. The mutant phenotype indicates a critical role for Gsh-1 in the genetic hierarchy of the formation and function of the hypothalamic-pituitary axis.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=8631293&retmode=ref&cmd=prlinks}, uri = {\url{papers3://publication/uuid/1C261762-0CEF-4CC2-ACB6-8E0A64B4B196}} }

@article{Valerius:1995ey, author = {Valerius, M T and Li, H and Stock, J L and Weinstein, M and Kaur, S and Singh, G and Potter, S S}, title = {{Gsh-1: a novel murine homeobox gene expressed in the central nervous system.}}, journal = {Developmental dynamics : an official publication of the American Association of Anatomists}, year = {1995}, volume = {203}, number = {3}, pages = {337--351}, month = jul, affiliation = {Division of Basic Science Research, Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Ohio 45229, USA.}, doi = {10.1002/aja.1002030306}, pmid = {8589431}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-06-06T21:51:15GMT}, date-modified = {2015-10-31T19:35:25GMT}, abstract = {We report the characterization of Gsh-1, a novel murine homeobox gene. Northern blot analysis revealed a transcript of approximately 2 kb in size present at embryonic days 10.5, 11.5, and 12.5 of development. The cDNA sequence encoded a proline rich motif, a polyalanine tract, and a homeodomain with strong homology to those encoded by the clustered Hox genes. The Gsh-1 expression pattern was determined for days E8.5 to E13.5 by whole mount and serial section in situ hybridizations. Gsh-1 transcription was restricted to the central nervous system. Expression is present in the neural tube and hindbrain as two continuous, bilaterally symmetrical stripes within neural epithelial tissue. In the mesencephalon, expression is seen as a band across the most anterior portion. There is also diencephalon expression in the anlagen of the thalamus and the hypothalamus as well as in the optic stalk, optic recess, and the ganglionic eminence. Moreover, through the use of fusion proteins containing the Gsh-1 homeodomain, we have determined the consensus DNA binding site of the Gsh-1 homeoprotein to be GCT/CA/CATTAG/A.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=8589431&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/1995/Valerius/Dev%20Dyn%201995%20Valerius.pdf}, file = {{Dev Dyn 1995 Valerius.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/1995/Valerius/Dev Dyn 1995 Valerius.pdf:application/pdf}}, uri = {\url{papers3://publication/doi/10.1002/aja.1002030306}} }

@article{Aronow:1995uo, author = {Aronow, B J and Ebert, C A and Valerius, M T and Potter, S S and Wiginton, D A and Witte, D P and Hutton, J J}, title = {{Dissecting a locus control region: facilitation of enhancer function by extended enhancer-flanking sequences.}}, journal = {Molecular and cellular biology}, year = {1995}, volume = {15}, number = {2}, pages = {1123--1135}, month = feb, affiliation = {Department of Pediatrics, Children's Hospital Medical Center, University of Cincinnati College of Medicine, Ohio 45229.}, pmid = {7823928}, pmcid = {PMC232021}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-08-06T14:28:21GMT}, date-modified = {2015-10-31T19:34:37GMT}, abstract = {Using transgenic mice, we have defined novel gene regulatory elements, termed "facilitators." These elements bilaterally flank, by up to 1 kb, a 200-bp T-cell-specific enhancer domain in the human adenosine deaminase (ADA) gene. Facilitators were essential for gene copy-proportional and integration site-independent reporter expression in transgenic thymocytes, but they had no effect on the enhancer in transfected T cells. Both segments were required. Individual segments had no activity. A lack of facilitator function caused positional susceptibility and prevented DNase I-hypersensitive site formation at the enhancer. The segments were required to be at opposed ends of the enhancer, and they could not be grouped together. Reversing the orientation of a facilitator segment caused a partial loss of function, suggesting involvement of a stereospecific chromatin structure. trans-acting factor access to enhancer elements was modeled by exposing nuclei to a restriction endonuclease. The enhancer domain was accessible to the 4-cutter DpnII in a tissue- and cell-type-specific fashion. However, unlike DNase I hypersensitivity and gene expression, accessibility to the endonuclease could occur without the facilitator segments, suggesting that an accessible chromatin domain is an intermediate state in the activational pathway. These results suggest that facilitators (i) are distinct from yet positionally constrained to the enhancer, (ii) participate in a chromatin structure transition that is necessary for the DNase I hypersensitivity and the transcriptional activating function of the enhancer, and (iii) act after cell-type-specific accessibility to the enhancer sequences is established by factors that do not require the facilitators to be present.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=7823928&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/1995/Aronow/Mol%20Cell%20Biol%201995%20Aronow.pdf}, file = {{Mol Cell Biol 1995 Aronow.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/1995/Aronow/Mol Cell Biol 1995 Aronow.pdf:application/pdf}}, uri = {\url{papers3://publication/uuid/462C8FF3-F319-43AC-AACF-3C68A510CB88}} }

@article{Kern:1992wm, author = {Kern, M J and Witte, D P and Valerius, M T and Aronow, B J and Potter, S S}, title = {{A novel murine homeobox gene isolated by a tissue specific PCR cloning strategy.}}, journal = {Nucleic acids research}, year = {1992}, volume = {20}, number = {19}, pages = {5189--5195}, month = oct, affiliation = {Childrens Hospital Research Foundation, Cincinnati, OH 45229.}, pmid = {1383943}, pmcid = {PMC334304}, language = {English}, read = {Yes}, rating = {0}, date-added = {2007-08-06T14:28:21GMT}, date-modified = {2015-10-27T15:59:13GMT}, abstract = {We have identified a novel homeobox gene, designated K-2, using a reverse transcription PCR cloning strategy. Sequence analysis reveals that the homeobox of K-2 is 77.6% homologous at the nucleotide level and 97% identical at the amino acid sequence level to another murine gene, S8. Homeodomain sequence comparisons indicate that K-2 and S8 represent a distinct subclass of paired type homeobox genes. Northern blot analysis of RNA from murine embryos and adult tissues identified multiple transcripts that are expressed in a developmentally specific and tissue restricted manner. Alternate splicing of K-2 at the 3-coding region leads to the inclusion of a chain terminating sequence. In addition, the developmental expression pattern of this gene at day 12 of gestation was determined by in situ hybridization. Expression was observed in diverse mesenchymal cells in craniofacial, pericardial, primitive dermal, prevertebral, and genital structures.}, url = {http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=1383943&retmode=ref&cmd=prlinks}, local-url = {file://localhost/Users/valerim/Dropbox%20(Partners%20HealthCare)/Dropbox%20(Partners%20HealthCare)/Papers3/Library.papers3/Articles/1992/Kern/Nucleic%20Acids%20Res%201992%20Kern.pdf}, file = {{Nucleic Acids Res 1992 Kern.pdf:/Users/valerim/Dropbox (Partners HealthCare)/Dropbox (Partners HealthCare)/Papers3/Library.papers3/Articles/1992/Kern/Nucleic Acids Res 1992 Kern.pdf:application/pdf}}, uri = {\url{papers3://publication/uuid/8AA67204-29AF-42A1-AB4E-AA9842ED2CB7}} }