Research Topics
Genomes and Genes
| Lothar HennighausenSummaryAffiliation: National Institutes of Health Country: USA Publications
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Detail Information
Publications
Conditional gene expression in secretory tissues and skin of transgenic mice using the MMTV-LTR and the tetracycline responsive systemL Hennighausen
Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, USA
J Cell Biochem 59:463-72. 1995..In addition, in combination with the CRE/lox recombination system, these mice wil be useful to achieve gene deletions at defined time points in these organs...- Information networks in the mammary glandLothar Hennighausen
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Rev Mol Cell Biol 6:715-25. 2005..Steroids and simple peptide hormones initiate and carry out complex developmental programmes, and reverse genetics has been used to define the underlying mechanistic connections... - Activation of beta-catenin in prostate epithelium induces hyperplasias and squamous transdifferentiationBrian Bierie
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Oncogene 22:3875-87. 2003..This suggests that the transdifferentiation into squamous metaplasias is an early response of endoderm-derived cells to beta-catenin, and that the development of intra-acinous hyperplasias or neoplastic foci is a later event... 
Inactivation of Stat5 in mouse mammary epithelium during pregnancy reveals distinct functions in cell proliferation, survival, and differentiationYongzhi Cui
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0822, USA
Mol Cell Biol 24:8037-47. 2004....- Identification of genes differentially expressed in mouse mammary epithelium transformed by an activated beta-cateninJean Pierre Renou
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Oncogene 22:4594-610. 2003..Lastly, stabilization of beta-catenin resulted in the retention of differentiated epithelium upon involution and altered activities of several proteases in transdifferentiated mammary epithelium... - Overexpression of the tumor suppressor gene phosphatase and tensin homologue partially inhibits wnt-1-induced mammary tumorigenesisHong Zhao
Diabetes Branch and Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892 1758, USA
Cancer Res 65:6864-73. 2005..This study identifies the PTEN as a therapeutic target for the treatment of mammary cancer and presumably other types of cancer... - Proteotyping of mammary tissue from transgenic and gene knockout mice with immunohistochemical markers: a tool to define developmental lesionsJonathan M Shillingford
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
J Histochem Cytochem 51:555-65. 2003..We propose that the technique of proteotyping will have wide applications in the analyses of defects in other mouse models... - Mammary epithelial cells are not able to undergo pregnancy-dependent differentiation in the absence of the helix-loop-helix inhibitor Id2Keiko Miyoshi
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases NIH, Building 8, Room 101, 8 Center Drive, Bethesda, MD 20892, USA
Mol Endocrinol 16:2892-901. 2002..From these results, we conclude that, in the absence of Id2, mammary epithelial development is arrested at an early stage of pregnancy... - The transcription factors STAT5A/B regulate GM-CSF-mediated granulopoiesisAkiko Kimura
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases NIDDK, National Institutes of Health NIH, Bethesda, MD, USA
Blood 114:4721-8. 2009..Finally, transcriptome analysis indicated that STAT5A/B directs GM-CSF signaling through the regulation of proliferation and survival genes... - The transcription factors signal transducer and activator of transcription 5A (STAT5A) and STAT5B negatively regulate cell proliferation through the activation of cyclin-dependent kinase inhibitor 2b (Cdkn2b) and Cdkn1a expressionJi Hoon Yu
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
Hepatology 52:1808-18. 2010..These experiments therefore shed mechanistic light on the context-specific role of STAT5 as tumor suppressor... - Hematopoietic-specific Stat5-null mice display microcytic hypochromic anemia associated with reduced transferrin receptor gene expressionBing Mei Zhu
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases NIDDKD, National Institutes of Health NIH, Bethesda, MD 20892, USA
Blood 112:2071-80. 2008..Chromatin immunoprecipitation experiments confirmed the binding of STAT5A/B to these sites. We conclude that STAT5A/B is an important regulator of iron update in erythroid progenitor cells via its control of Tfr1 transcription... - Mammary gland remodeling depends on gp130 signaling through Stat3 and MAPKLing Zhao
Laboratory of Genetics and Physiology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 279:44093-100. 2004..These experiments establish that two distinct Stat3 signaling pathways emanating from gp130 are utilized in mammary tissue... - Interleukin-2 signaling via STAT5 constrains T helper 17 cell generationArian Laurence
Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 26:371-81. 2007..We conclude that in addition to the promotion of activation-induced cell death of lymphocytes and the generation of Treg cells, inhibition of Th17 polarization appears to be an important function of IL-2... - Squamous cell carcinoma and mammary abscess formation through squamous metaplasia in Smad4/Dpc4 conditional knockout miceWenmei Li
Genetics of Development and Disease Branch, NIDDK, NIH, 10 9N105, 10 Center Drive, Bethesda, MD 20892, USA
Development 130:6143-53. 2003..However, such actions were blocked in the absence of Smad4. These findings indicate that TGFbeta/Smad4 signals play a role in cell fate maintenance during mammary gland development and neoplasia... - Socs 3 modulates the activity of the transcription factor Stat3 in mammary tissue and controls alveolar homeostasisGertraud W Robinson
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0822, USA
Dev Dyn 236:654-61. 2007..Loss of Socs3 led to enhanced and precocious Stat3 activation. Thus, Socs3 serves as a modulator of Stat3 activity to ensure controlled proliferation and apoptosis in pregnancy and involution, respectively... - Loss of interleukin 6 results in delayed mammary gland involution: a possible role for mitogen-activated protein kinase and not signal transducer and activator of transcription 3Ling Zhao
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, and Hematology Branch NIH, Building 8 Room 101, 8 Center Drive, Bethesda, MD 20892, USA
Mol Endocrinol 16:2902-12. 2002.... - Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cellsMartin Guimond
Pediatric Oncology Branch, National Cancer Institute, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 10:149-57. 2009..Our results indicate that IL-7Ralpha(+) DCs are regulators of the peripheral CD4(+) T cell niche and that IL-7 signals in DCs prevent uncontrolled CD4(+) T cell population expansion in vivo... 
SOCS3 negatively regulates the gp130-STAT3 pathway in mouse skin wound healingBing Mei Zhu
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
J Invest Dermatol 128:1821-9. 2008..These results demonstrate that wound healing is controlled in keratinocytes by the gp130-SOCS3-STAT3 pathway and an imbalance of this pathway results in delayed wound healing...- Selective removal of the selenocysteine tRNA [Ser]Sec gene (Trsp) in mouse mammary epitheliumEaswari Kumaraswamy
Section on Molecular Biology of Selenium, Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Cell Biol 23:1477-88. 2003..Thus, the conditional Trsp knockout mouse allows tissue-specific manipulation of Sec tRNA and selenoprotein expression, suggesting that this approach will provide a useful tool for studying the role of selenoproteins in health... - The gene encoding the hematopoietic stem cell regulator CCN3/NOV is under direct cytokine control through the transcription factors STAT5A/BAkiko Kimura
Laboratory of Genetics and Physiology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 285:32704-9. 2010..ChIP assays using 32D cells revealed IL-3-induced binding of STAT5A/B to a γ-interferon-activated sequences site in the Ccn3/Nov gene promoter. This is the first report that Ccn3/Nov is directly induced by cytokines through STAT5A/B... - Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5ADaisuke Yamaji
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Genes Dev 23:2382-7. 2009..Thus, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells... - The transcription factors Stat5a/b are not required for islet development but modulate pancreatic beta-cell physiology upon agingJi Yeon Lee
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 8 Center Drive, Room 101, Bethesda, MD 20892 0822, USA
Biochim Biophys Acta 1773:1455-61. 2007..Mild glucose intolerance occurred with age. We conclude that Stat5 is not essential for islet development but may modulate beta-cell function... - SOCS3 promotes apoptosis of mammary differentiated cellsFabienne Le Provost
Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
Biochem Biophys Res Commun 338:1696-701. 2005..Together, our results are consistent with a role of SOCS3 in the mammary gland by promoting apoptosis of differentiated cells (adipocytes during gestation and epithelial cells during involution)... - Signaling by intrathymic cytokines, not T cell antigen receptors, specifies CD8 lineage choice and promotes the differentiation of cytotoxic-lineage T cellsJung Hyun Park
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
Nat Immunol 11:257-64. 2010.... - Loss of STAT5 causes liver fibrosis and cancer development through increased TGF-{beta} and STAT3 activationAtsushi Hosui
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Exp Med 206:819-31. 2009..In conclusion, loss of STAT5 results in elevated TGF-beta levels and enhanced growth hormone-induced STAT3 activity. We propose that a deregulated STAT5-TGF-beta-STAT3 network contributes to the development of chronic liver disease... - Skeletal muscle growth and fiber composition in mice are regulated through the transcription factors STAT5a/b: linking growth hormone to the androgen receptorPeter Klover
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
FASEB J 23:3140-8. 2009..These experiments demonstrate an important role for STAT5a/b in skeletal muscle physiology, and they provide a direct link to androgen signaling... - The canonical Notch/RBP-J signaling pathway controls the balance of cell lineages in mammary epithelium during pregnancyKrista D Buono
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Dev Biol 293:565-80. 2006..We propose that the Notch-RBP-J pathway regulates alveolar development during pregnancy by maintaining luminal cell fate and preventing uncontrolled basal cell proliferation... - Bcl-x is not required for maintenance of follicles and corpus luteum in the postnatal mouse ovaryGregory Riedlinger
Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Biol Reprod 66:438-44. 2002..Whereas luteal cells underwent apoptosis in the absence of the PrlR, no changes were observed in the absence of Stat5 or Bcl-x... - Nonredundant roles for Stat5a/b in directly regulating Foxp3Zhengju Yao
Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892 1820, USA
Blood 109:4368-75. 2007..Therefore, we conclude that Stat5a/b have an essential, nonredundant role in regulating Treg cells, and that Stat3 and Stat5a/b appear to have opposing roles in the regulation of Foxp3... - PTEN overexpression suppresses proliferation and differentiation and enhances apoptosis of the mouse mammary epitheliumJoelle Dupont
Section on Molecular and Cellular Physiology, Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892, USA
J Clin Invest 110:815-25. 2002..MK-PTEN mice also exhibited a 50% decrease in the phosphorylation state of Akt. Taken together, these results suggest that PTEN controls mammary gland development and, consequently, lactation... - Loss of signal transducer and activator of transcription 5 leads to hepatosteatosis and impaired liver regenerationYongzhi Cui
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892 0822, USA
Hepatology 46:504-13. 2007..CONCLUSION: Aberrant cytokine-Stat5 signaling in hepatocytes alters their physiology through increased activity of Stat1 and Stat3. Such cross-talk between different pathways could add to the complexity of syndromes observed in disease... - Loss of connexin 26 in mammary epithelium during early but not during late pregnancy results in unscheduled apoptosis and impaired developmentCeline Bry
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Dev Biol 267:418-29. 2004..Cx26 is considered a tumor suppressor gene and Cx26-null mammary tissue was evaluated after five pregnancies. No hyperproliferation or hyperplasia was observed, suggesting that Cx26 does not function as a tumor suppressor... - Smad3 in the mammary epithelium has a nonredundant role in the induction of apoptosis, but not in the regulation of proliferation or differentiation by transforming growth factor-betaYu An Yang
Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892 5055, USA
Cell Growth Differ 13:123-30. 2002..The results suggest that epithelial Smad3 is dispensable for TGF-beta effects on proliferation and differentiation in the mammary gland, but that it contributes in a nonredundant manner to the induction of apoptosis... - Biogenesis and function of mouse mammary epithelium depends on the presence of functional alpha-cateninRashmi V Nemade
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 8, Room 101, 8 Center Drive, Bethesda, MD 20892, USA
Mech Dev 121:91-9. 2004..Lastly, no tumors were detected in mammary tissue lacking alpha-catenin... - Deletion of Stat3 blocks mammary gland involution and extends functional competence of the secretory epithelium in the absence of lactogenic stimuliRobin C Humphreys
Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Endocrinology 143:3641-50. 2002..Our data demonstrate that mammary tissue can retain its functional competence in the absence of external lactogenic stimuli and demonstrate a delay in the initiation of the irreversible stage of involution... - Mouse mammary epithelial cells express the Na-K-Cl cotransporter, NKCC1: characterization, localization, and involvement in ductal development and morphogenesisJonathan M Shillingford
Laboratory of Genetics and Physiology, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Endocrinol 16:1309-21. 2002.... - Activation of different Wnt/beta-catenin signaling components in mammary epithelium induces transdifferentiation and the formation of pilar tumorsKeiko Miyoshi
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, MD 20892, USA
Oncogene 21:5548-56. 2002.... - Targeted expression of HGF/SF in mouse mammary epithelium leads to metastatic adenosquamous carcinomas through the activation of multiple signal transduction pathwaysMarta I Gallego
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0822, USA
Oncogene 22:8498-508. 2003..We suggest that these mice may serve as a new breast cancer model for the evaluation of the effects of unscheduled HGF expression in breast cancer... - Loss of cytokine-STAT5 signaling in the CNS and pituitary gland alters energy balance and leads to obesityJi Yeon Lee
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
PLoS ONE 3:e1639. 2008..These results demonstrate that STAT5 mediates energy homeostasis in response to endogenous cytokines such as GM-CSF... - The aryl hydrocarbon receptor (AhR) and its nuclear translocator (Arnt) are dispensable for normal mammary gland development but are required for fertilityFabienne Le Provost
Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0822, USA
Genesis 32:231-9. 2002..Normal mammary structures were observed in the absence of Arnt and AhR, demonstrating that neither transcription factor is necessary for mammary development... - Stat5a/b are essential for normal lymphoid development and differentiationZhengju Yao
Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 103:1000-5. 2006..Thus, deficiency of Stat5 results in severe combined immunodeficiency, similar in many respects to deficiency of IL-7R, gammac, and Jak3... - Genome-wide analyses reveal the extent of opportunistic STAT5 binding that does not yield transcriptional activation of neighboring genesBing Mei Zhu
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Nucleic Acids Res 40:4461-72. 2012..Up to 40% of STAT5-bound genes were not expressed. For the first time we demonstrate the magnitude of opportunistic genomic STAT5 binding that does not translate into transcriptional activation of neighboring genes... - Postnatal body growth is dependent on the transcription factors signal transducers and activators of transcription 5a/b in muscle: a role for autocrine/paracrine insulin-like growth factor IPeter Klover
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 8 Center Drive, Building 8, Room 107, Bethesda, Maryland 20892 0822, USA
Endocrinology 148:1489-97. 2007..These results demonstrate an as yet unreported critical role for STAT5 in skeletal muscle for local IGF-I production and postnatal growth and suggest the skeletal muscle as a major site of GH action... - Growth hormone-STAT5 regulation of growth, hepatocellular carcinoma, and liver metabolismMyunggi Baik
Laboratory of Genetics and Physiology, National Institutes of Health, Bethesda, Maryland, USA
Ann N Y Acad Sci 1229:29-37. 2011..Finally, we discuss recent discoveries about the role of GH-STAT5 in sex-specific gene expression and bile acid, steroid, and drug metabolism... - MMTV-Cre transgenes can adversely affect lactation: considerations for conditional gene deletion in mammary tissueGertraud W Robinson
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Anal Biochem 412:92-5. 2011..This study demonstrates the importance of including appropriate "Cre-only" controls and provides guidelines to avoid problems in data interpretation... - The proliferation associated nuclear element (PANE1) is conserved between mammals and fish and preferentially expressed in activated lymphoid cellsBrian Bierie
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 8, Room 101, Bethesda, MD 20892 0822, USA
Gene Expr Patterns 4:389-95. 2004..In B- and T-cells PANE1 RNA was only detected after the respective cell types were activated either in vivo or in vitro... - Activation of beta -catenin signaling in differentiated mammary secretory cells induces transdifferentiation into epidermis and squamous metaplasiasKeiko Miyoshi
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 99:219-24. 2002..These data demonstrate that the activation of beta-catenin signaling induces a program that results in loss of mammary epithelial cell differentiation and induction of epidermal structures... - The miR-17/92 cluster is targeted by STAT5 but dispensable for mammary developmentYonatan Feuermann
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Genesis 50:665-71. 2012..Our studies demonstrated that, while expression of the miR-17/92 cluster is under control of the key mammary transcription factor STAT5, its presence is not required for normal mammary development or lactation... - Differential requirements for shh in mammary tissue and hair follicle morphogenesisMarta I Gallego
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, Maryland 20892, USA
Dev Biol 249:131-9. 2002.... - Selective regulatory function of Socs3 in the formation of IL-17-secreting T cellsZhi Chen
Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 103:8137-42. 2006..We conclude that Socs3 is an essential negative regulator of IL-23 signaling, inhibition of which constrains the generation of Th17 differentiation... - RIP-Cre revisited, evidence for impairments of pancreatic beta-cell functionJi-Yeon Lee
Laboratory of Genetics and Physiology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 281:2649-53. 2006..In addition, we review the use of RIP-Cre mice and discuss possible molecular underpinnings and ramifications of our findings... - A morphological and immunohistochemical comparison of mammary tissues from the short-tailed fruit bat (Carollia perspicillata) and the mouseJennifer L Evarts
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Biol Reprod 70:1573-9. 2004..The present study demonstrates that whereas the epithelial compartment and the presence of differentiation markers are conserved between the mouse and bat, differences exist in the stromal compartment... - Reduced circulating insulin-like growth factor I levels delay the onset of chemically and genetically induced mammary tumorsYiping Wu
Section on Cellular and Molecular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases NIH, Building 10, Bethesda, MD 20892, USA
Cancer Res 63:4384-8. 2003..Our data demonstrate that circulating IGF-I levels play a significant role as a risk factor in the onset and development of mammary tumors in two well-established animal models of breast cancer... - The transcription factor Stat3 is dispensable for pancreatic beta-cell development and functionJi Yeon Lee
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Biochem Biophys Res Commun 334:764-8. 2005..The finding that RIP-Cre transgenic mice in a C57B/6 dominated background develop glucose intolerance is important as this line has been used in several studies... - The liver-specific tumor suppressor STAT5 controls expression of the reactive oxygen species-generating enzyme NOX4 and the proapoptotic proteins PUMA and BIM in miceJi Hoon Yu
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892 0822, USA
Hepatology 56:2375-86. 2012..Besides suppressing the activation of STAT3, STAT5 induces the expression of proapoptotic genes and the production of ROS... - Loss of STAT1 from mouse mammary epithelium results in an increased Neu-induced tumor burdenPeter J Klover
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
Neoplasia 12:899-905. 2010..The Stat1 floxed allele described in this study is also a unique resource to determine the cellular targets of IFNs and STAT1 action, which should aid our understanding and appreciation of these pathways... - Loss of the peroxisome proliferation-activated receptor gamma (PPARgamma ) does not affect mammary development and propensity for tumor formation but leads to reduced fertilityYongzhi Cui
Laboratory of Genetics and Physiology, NIDDK, the Laboratory of Immunoregulation, Immune Activation Section, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 277:17830-5. 2002..These mice have normal populations of follicles, they ovulate and develop corpora lutea. Although progesterone levels are decreased and implantation rates are reduced, the exact cause of the impaired fertility remains to be determined... - Genomic dissection of the cytokine-controlled STAT5 signaling network in liverAtsushi Hosui
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0822, USA
Physiol Genomics 34:135-43. 2008..We also explore whether this wealth of information on gene activity can be used to further understand the roles of cytokines in liver disease... - Interpretation of cytokine signaling through the transcription factors STAT5A and STAT5BLothar Hennighausen
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Genes Dev 22:711-21. 2008..We propose that mice with mutations in various components of the JAK-STAT signaling pathway are living laboratories, which will provide insight into the versatility of signaling hardware and the adaptability of the software... - EZH2 methyltransferase and H3K27 methylation in breast cancerKyung Hyun Yoo
Laboratory of Genetics and Physiology, National Institutes of Health, Bethesda, MD 20892, USA
Int J Biol Sci 8:59-65. 2012..We also discuss distinct molecular mechanisms used by EZH2 to suppress BRCA1 functions... - Jak2 is an essential tyrosine kinase involved in pregnancy-mediated development of mammary secretory epitheliumJonathan M Shillingford
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Endocrinol 16:563-70. 2002..Taken together, our results demonstrate that Jak2 is a critical tyrosine kinase that conveys intracellular signals necessary for proliferation and differentiation of mammary epithelium during pregnancy... - Validation of transgenic mammary cancer models: goals of the NCI Mouse Models of Human Cancer Consortium and the mammary cancer CD-ROMJeffrey E Green
Laboratory of Cellular Regulation and Carcinogenesis, National Cancer Institute, Building 41, Bethesda, MD 20892, USA
Transgenic Res 11:635-6. 2002 - Circulating insulin-like growth factor-I levels regulate colon cancer growth and metastasisYiping Wu
Section of Cellular and Molecular Physiology, Cellular Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892-1758, USA
Cancer Res 62:1030-5. 2002..This study supports the hypothesis that circulating IGF-I levels play an important role in tumor development and metastasis... - Identification of an acquired mutation in Jak2 provides molecular insights into the pathogenesis of myeloproliferative disordersMarko Pesu
Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Mol Interv 5:211-5. 2005 - Direct glucocorticoid receptor-Stat5 interaction in hepatocytes controls body size and maturation-related gene expressionDavid Engblom
Division of Molecular Biology of the Cell I, German Cancer Research Center, D 69120 Heidelberg, Germany
Genes Dev 21:1157-62. 2007..This interaction mediates a selective and unexpectedly extensive part of the transcriptional actions of these molecules since it controls the expression of gene sets involved in growth and sexual maturation... - Impaired differentiation and lactational failure of Erbb4-deficient mammary glands identify ERBB4 as an obligate mediator of STAT5Weiwen Long
Department of Structural and Cellular Biology, Tulane Cancer Center, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, Louisiana 70112 2699, USA
Development 130:5257-68. 2003.... - The cyclin-dependent kinase inhibitor p27 (Kip1) regulates both DNA synthesis and apoptosis in mammary epithelium but is not required for its functional development during pregnancyElizabeth A Davison
Cancer Research Program, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, New South Wales 2010, Australia
Mol Endocrinol 17:2436-47. 2003..However, the absence of morphological and cellular defects in p27-/- mammary tissue during pregnancy raises the possibility that loss of p27 in breast cancer may not confer an overall growth advantage unless apoptosis is also impaired... - Conditional loss of PTEN leads to precocious development and neoplasia in the mammary glandGang Li
Department of Molecular and Medical Pharmacology, UCLA School of Medicine, 650 Circle Drive South, 90095 1735, USA
Development 129:4159-70. 2002.... - GFP expression in the mammary gland for imaging of mammary tumor cells in transgenic miceFayyaz Ahmed
Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
Cancer Res 62:7166-9. 2002..These animals provide a range of expression of GFP that is suitable for analysis of transgenic mammary tumors and metastases in vivo at the single cell level of resolution... - Tsg101 is essential for cell growth, proliferation, and cell survival of embryonic and adult tissuesKay Uwe Wagner
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha 68198 6805, USA
Mol Cell Biol 23:150-62. 2003..In summary, our results suggest that Tsg101 is required for normal cell function of embryonic and adult tissues but that this gene is not a tumor suppressor for sporadic forms of breast cancer... - Disruption of steroid and prolactin receptor patterning in the mammary gland correlates with a block in lobuloalveolar developmentSandra L Grimm
Department of Molecular and Cellular Biology, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA
Mol Endocrinol 16:2675-91. 2002..Together, these data suggest that C/EBPbeta is a master regulator of mammary epithelial cell fate and that the correct spatial pattern of PR and PrlR expression is a critical determinant of hormone-regulated cell proliferation... - An adjunct mammary epithelial cell population in parous females: its role in functional adaptation and tissue renewalKay Uwe Wagner
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Rm 8009, Omaha, NE 68198 6805, USA
Development 129:1377-86. 2002..e. ductal morphogenesis and lobulogenesis). We propose that this parity-induced population contributes importantly to the biological differences between the mammary glands of parous and nulliparous females... - Early onset of neoplasia in the prostate and skin of mice with tissue-specific deletion of PtenStephanie A Backman
Department of Medical Biophysics, University of Toronto, Ontario Cancer Institute and University Health Network, 610 University Avenue, Toronto, Ontario, Canada M5G 2M9
Proc Natl Acad Sci U S A 101:1725-30. 2004..Consistent with high PTEN mutation rates in human prostate tumors, these data indicate that PTEN is a critical tumor suppressor in this organ... - Brca2 deficiency does not impair mammary epithelium development but promotes mammary adenocarcinoma formation in p53(+/-) mutant miceAlison M Y Cheung
Advanced Medical Discovery Institute, University Health Network, 620 University Avenue, Suite 706, Toronto, Ontario M5G 2C1, Canada
Cancer Res 64:1959-65. 2004..Our data indicate that Brca2 is not essential for mammary epithelium development but that Brca2 deficiency and down-regulated p53 expression can work jointly to promote mammary tumorigenesis... - Development of the mammary gland requires DGAT1 expression in stromal and epithelial tissuesSylvaine Cases
Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141 1900, USA
Development 131:3047-55. 2004..Our findings are the first to link defects in stromal lipid metabolism to impaired mammary gland development... - Loss of sexually dimorphic liver gene expression upon hepatocyte-specific deletion of Stat5a-Stat5b locusMinita G Holloway
Department of Biology, Boston University, Boston, Massachusetts 02215, USA
Endocrinology 148:1977-86. 2007..Thus, the major loss of liver sexual dimorphism in hepatocyte STAT5ab-deficient mice can primarily be attributed to the loss of STAT5b... - Stat5 is essential for early B cell development but not for B cell maturation and functionXuezhi Dai
State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, People s Republic of China
J Immunol 179:1068-79. 2007..Taken together, these data demonstrate that Stat5A/5B directly control IL-7-mediated early B cell development but are not required for B cell maturation and Ig production... - Helper T cell IL-2 production is limited by negative feedback and STAT-dependent cytokine signalsAlejandro V Villarino
Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA
J Exp Med 204:65-71. 2007.... - STAT5 requires the N-domain to maintain hematopoietic stem cell repopulating function and appropriate lymphoid-myeloid lineage outputGeqiang Li
Department of Medicine, Division of Hematology Oncology, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, USA
Exp Hematol 35:1684-94. 2007..The goal of these studies was to use transplantation-based assays to analyze the degree of STAT5 deltaN activity in hematopoietic stem cells (HSC) and throughout lymphomyeloid development... - Epithelial-specific and stage-specific functions of insulin-like growth factor-I during postnatal mammary developmentAimee V Loladze
Department of Neural and Behavioral Sciences, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA
Endocrinology 147:5412-23. 2006..Taken together, our results support distinct roles for IGF-I expressed in epithelial and stromal compartments in mediating growth of the postnatal mammary gland... - Acute myeloid leukemia-associated Mkl1 (Mrtf-a) is a key regulator of mammary gland functionYi Sun
Department of Pathology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Mol Cell Biol 26:5809-26. 2006..Despite the importance of Srf in multiple transcriptional pathways and widespread Mkl1 expression, the spectrum of abnormalities associated with Mkl1 absence appears surprisingly restricted... - Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformationAndrea Hoelbl
Institute of Pharmacology, Medical University of Vienna, A 1090 Vienna, Austria
Blood 107:4898-906. 2006..These findings show distinct lymphoid defects for Stat5a/b(DeltaN/DeltaN) and Stat5a/b(null/null) mice and define a novel functional role for the N-termini of Stat5a/b in B-lymphoid transformation... - C/EBPdelta is a crucial regulator of pro-apoptotic gene expression during mammary gland involutionMuthusamy Thangaraju
Laboratory of Protein Dynamics and Signaling, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702 1201, USA
Development 132:4675-85. 2005..This study places C/EBPdelta between STAT3 and several pro- and anti-apoptotic genes promoting the physiological cell death response in epithelial cells at the onset of mammary gland involution... - Genetic evidence supporting selection of the Valpha14i NKT cell lineage from double-positive thymocyte precursorsTakeshi Egawa
Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA
Immunity 22:705-16. 2005..Our results indicate that even though CD1d binding DP thymocytes have yet to be observed, Valpha14-Jalpha18 rearrangement in these cells is required for development of iNKT cells... - Activation of PPAR gamma and delta by conjugated linoleic acid mediates protection from experimental inflammatory bowel diseaseJosep Bassaganya-Riera
Laboratory of Nutritional Immunology and Molecular Nutrition, Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061, USA
Gastroenterology 127:777-91. 2004..We used a loss-of-function approach to investigate whether CLA ameliorated colitis through a peroxisome proliferator-activated receptor gamma (PPAR gamma)-dependent mechanism... - SOCS3 protein developmentally regulates the chemokine receptor CXCR4-FAK signaling pathway during B lymphopoiesisYi Le
Children s Hospital Boston and Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115, USA
Immunity 27:811-23. 2007..We propose that the developmental regulation of CXCR4-FAK signaling by SOCS3 is an important mechanism to control the lodgement of B cell precursors in the BM microenvironment...