Lothar Hennighausen

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Beta-catenin: a transforming actor on many stages
    Keiko Miyoshi
    Department of Biochemistry, School of Dentistry, The University of Tokushima, Japan
    Breast Cancer Res 5:63-8. 2003
  2. pmc Interpretation of cytokine signaling through the transcription factors STAT5A and STAT5B
    Lothar 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
  3. ncbi request reprint Activation of beta-catenin in prostate epithelium induces hyperplasias and squamous transdifferentiation
    Brian 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
  4. ncbi request reprint Proteotyping of mammary tissue from transgenic and gene knockout mice with immunohistochemical markers: a tool to define developmental lesions
    Jonathan 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
  5. ncbi request reprint Identification of genes differentially expressed in mouse mammary epithelium transformed by an activated beta-catenin
    Jean 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
  6. pmc Inactivation of Stat5 in mouse mammary epithelium during pregnancy reveals distinct functions in cell proliferation, survival, and differentiation
    Yongzhi 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
  7. ncbi request reprint Overexpression of the tumor suppressor gene phosphatase and tensin homologue partially inhibits wnt-1-induced mammary tumorigenesis
    Hong 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
  8. ncbi request reprint Mammary epithelial cells are not able to undergo pregnancy-dependent differentiation in the absence of the helix-loop-helix inhibitor Id2
    Keiko 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
  9. pmc The transcription factors STAT5A/B regulate GM-CSF-mediated granulopoiesis
    Akiko 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
  10. pmc 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 expression
    Ji 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

Collaborators

Detail Information

Publications127 found, 100 shown here

  1. pmc Beta-catenin: a transforming actor on many stages
    Keiko Miyoshi
    Department of Biochemistry, School of Dentistry, The University of Tokushima, Japan
    Breast Cancer Res 5:63-8. 2003
    ..Although there is evidence for a contextual specificity of the Wnt signaling, the experimental systems and designs used in different studies probably influence the cellular responses...
  2. pmc Interpretation of cytokine signaling through the transcription factors STAT5A and STAT5B
    Lothar 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...
  3. ncbi request reprint Activation of beta-catenin in prostate epithelium induces hyperplasias and squamous transdifferentiation
    Brian 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...
  4. ncbi request reprint Proteotyping of mammary tissue from transgenic and gene knockout mice with immunohistochemical markers: a tool to define developmental lesions
    Jonathan 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...
  5. ncbi request reprint Identification of genes differentially expressed in mouse mammary epithelium transformed by an activated beta-catenin
    Jean 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...
  6. pmc Inactivation of Stat5 in mouse mammary epithelium during pregnancy reveals distinct functions in cell proliferation, survival, and differentiation
    Yongzhi 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
    ....
  7. ncbi request reprint Overexpression of the tumor suppressor gene phosphatase and tensin homologue partially inhibits wnt-1-induced mammary tumorigenesis
    Hong 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...
  8. ncbi request reprint Mammary epithelial cells are not able to undergo pregnancy-dependent differentiation in the absence of the helix-loop-helix inhibitor Id2
    Keiko 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...
  9. pmc The transcription factors STAT5A/B regulate GM-CSF-mediated granulopoiesis
    Akiko 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...
  10. pmc 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 expression
    Ji 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
    ..We now establish that STAT5, like in MEFs, activates expression of the Cdkn2b gene in liver tissue. Loss of STAT5 led to diminished p15(INK4B) and increased hepatocyte proliferation...
  11. pmc The liver-specific tumor suppressor STAT5 controls expression of the reactive oxygen species-generating enzyme NOX4 and the proapoptotic proteins PUMA and BIM in mice
    Ji 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
    ..This study demonstrates for the first time that cytokines through STAT5 regulate the expression of the ROS-generating enzyme NOX4 and key proapoptotic proteins...
  12. ncbi request reprint Prolactin, growth hormone, and epidermal growth factor activate Stat5 in different compartments of mammary tissue and exert different and overlapping developmental effects
    M I Gallego
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA
    Dev Biol 229:163-75. 2001
    ..Our findings demonstrate that GH, Prl, and EGF activate Stat5 in separate compartments, which in turn reflects their specific roles in ductal and alveolar development and differentiation...
  13. ncbi request reprint Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation
    Arian 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...
  14. pmc Hematopoietic-specific Stat5-null mice display microcytic hypochromic anemia associated with reduced transferrin receptor gene expression
    Bing 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...
  15. ncbi request reprint 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 3
    Ling 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
    ....
  16. ncbi request reprint Squamous cell carcinoma and mammary abscess formation through squamous metaplasia in Smad4/Dpc4 conditional knockout mice
    Wenmei 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...
  17. ncbi request reprint Mammary gland remodeling depends on gp130 signaling through Stat3 and MAPK
    Ling 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...
  18. ncbi request reprint Structure of the mouse Stat 3/5 locus: evolution from Drosophila to zebrafish to mouse
    K Miyoshi
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Building 8, Room 101, Bethesda, Maryland 20892, USA
    Genomics 71:150-5. 2001
    ..We propose that the Stat3 and Stat5 lineages are derived from the duplication of a common primordial gene and that d-Stat is a part of the Stat5 lineage...
  19. ncbi request reprint Socs 3 modulates the activity of the transcription factor Stat3 in mammary tissue and controls alveolar homeostasis
    Gertraud 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...
  20. ncbi request reprint SOCS3 promotes apoptosis of mammary differentiated cells
    Fabienne 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)...
  21. ncbi request reprint Conditional deletion of the bcl-x gene from mouse mammary epithelium results in accelerated apoptosis during involution but does not compromise cell function during lactation
    K D Walton
    Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Mech Dev 109:281-93. 2001
    ..Concomitant deletion of the bax gene did not significantly modify the Bcl-x phenotype. Our results suggest that Bcl-x is not essential during mammopoiesis, but is critical for controlled apoptosis during the first phase of involution...
  22. pmc Mammary-specific gene activation is defined by progressive recruitment of STAT5 during pregnancy and the establishment of H3K4me3 marks
    Keunsoo Kang
    Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Mol Cell Biol 34:464-73. 2014
    ..This is the first study in an organ that links progressive chromatin occupancy of STAT5 to the acquisition of H3K4me3 marks and transcription during hormone-induced differentiation. ..
  23. pmc Selective removal of the selenocysteine tRNA [Ser]Sec gene (Trsp) in mouse mammary epithelium
    Easwari 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...
  24. ncbi request reprint Jak2 is an essential tyrosine kinase involved in pregnancy-mediated development of mammary secretory epithelium
    Jonathan 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...
  25. ncbi request reprint Deletion of Stat3 blocks mammary gland involution and extends functional competence of the secretory epithelium in the absence of lactogenic stimuli
    Robin 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...
  26. pmc PTEN overexpression suppresses proliferation and differentiation and enhances apoptosis of the mouse mammary epithelium
    Joelle 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...
  27. pmc Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5A
    Daisuke 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...
  28. pmc The gene encoding the hematopoietic stem cell regulator CCN3/NOV is under direct cytokine control through the transcription factors STAT5A/B
    Akiko 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...
  29. pmc Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cells
    Martin 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...
  30. ncbi request reprint Expression of a truncated Int3 gene in developing secretory mammary epithelium specifically retards lobular differentiation resulting in tumorigenesis
    D Gallahan
    Laboratory of Tumor Immunology and Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Cancer Res 56:1775-85. 1996
    ....
  31. ncbi request reprint Mouse mammary epithelial cells express the Na-K-Cl cotransporter, NKCC1: characterization, localization, and involvement in ductal development and morphogenesis
    Jonathan M Shillingford
    Laboratory of Genetics and Physiology, National Institutes of Health, Bethesda, Maryland 20892, USA
    Mol Endocrinol 16:1309-21. 2002
    ....
  32. pmc The transcription factors Stat5a/b are not required for islet development but modulate pancreatic beta-cell physiology upon aging
    Ji 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...
  33. pmc Skeletal muscle growth and fiber composition in mice are regulated through the transcription factors STAT5a/b: linking growth hormone to the androgen receptor
    Peter 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...
  34. pmc Loss of STAT5 causes liver fibrosis and cancer development through increased TGF-{beta} and STAT3 activation
    Atsushi 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...
  35. ncbi request reprint The canonical Notch/RBP-J signaling pathway controls the balance of cell lineages in mammary epithelium during pregnancy
    Krista 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...
  36. pmc Signaling by intrathymic cytokines, not T cell antigen receptors, specifies CD8 lineage choice and promotes the differentiation of cytotoxic-lineage T cells
    Jung Hyun Park
    Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    Nat Immunol 11:257-64. 2010
    ....
  37. ncbi request reprint Activation of different Wnt/beta-catenin signaling components in mammary epithelium induces transdifferentiation and the formation of pilar tumors
    Keiko 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
    ....
  38. ncbi request reprint SOCS3 negatively regulates the gp130-STAT3 pathway in mouse skin wound healing
    Bing 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...
  39. ncbi request reprint Loss of signal transducer and activator of transcription 5 leads to hepatosteatosis and impaired liver regeneration
    Yongzhi 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...
  40. ncbi request reprint Loss of connexin 26 in mammary epithelium during early but not during late pregnancy results in unscheduled apoptosis and impaired development
    Celine 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...
  41. ncbi request reprint 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-beta
    Yu 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...
  42. ncbi request reprint The aryl hydrocarbon receptor (AhR) and its nuclear translocator (Arnt) are dispensable for normal mammary gland development but are required for fertility
    Fabienne 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...
  43. ncbi request reprint Reduced circulating insulin-like growth factor I levels delay the onset of chemically and genetically induced mammary tumors
    Yiping 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...
  44. pmc Nonredundant roles for Stat5a/b in directly regulating Foxp3
    Zhengju 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...
  45. ncbi request reprint Epithelial defect in prostates of Stat5a-null mice
    M T Nevalainen
    Department of Pathology, Uniformed Services University of the Health Sciences, and National Institutes of Diabetes and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Lab Invest 80:993-1006. 2000
    ..The present study offers the first evidence for a direct role of Stat5a in the maintenance of normal tissue architecture and function of the mouse prostate...
  46. ncbi request reprint Role of serine phosphorylation of Stat5a in prolactin-stimulated beta-casein gene expression
    H Yamashita
    United States Military Cancer Institute, Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Mol Cell Endocrinol 183:151-63. 2001
    ..We propose that serine phosphorylation within the transactivation domain may limit the activity of Stat5a in the absence of proper coactivation by glucocorticoid receptors...
  47. ncbi request reprint Functional rescue of Stat5a-null mammary tissue through the activation of compensating signals including Stat5b
    X Liu
    Laboratory of Genetics and Physiology, National Institutes of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892, USA
    Cell Growth Differ 9:795-803. 1998
    ..These experiments demonstrate that the mammary gland has inherent plasticity that allows it to use different signals to achieve its ultimate purpose, the production of milk to nurture newborn offspring...
  48. pmc Stat5a/b are essential for normal lymphoid development and differentiation
    Zhengju 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...
  49. pmc Genome-wide analyses reveal the extent of opportunistic STAT5 binding that does not yield transcriptional activation of neighboring genes
    Bing 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...
  50. pmc Sequential activation of genetic programs in mouse mammary epithelium during pregnancy depends on STAT5A/B concentration
    Daisuke Yamaji
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20815, USA
    Nucleic Acids Res 41:1622-36. 2013
    ..RNA polymerase II intensity was directly proportional to STAT5 concentration only on STAT5 regulated genes providing mechanistic insight by which STAT5 activates mammary specific genes...
  51. pmc Biogenesis and function of mouse mammary epithelium depends on the presence of functional alpha-catenin
    Rashmi 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...
  52. ncbi request reprint Targeted expression of HGF/SF in mouse mammary epithelium leads to metastatic adenosquamous carcinomas through the activation of multiple signal transduction pathways
    Marta 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...
  53. pmc Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue
    X Liu
    Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 92:8831-5. 1995
    ..The increase of Stat5 expression during pregnancy coincides with the activation of the WAP gene...
  54. ncbi request reprint Genomic architecture and transcriptional activation of the mouse and human tumor susceptibility gene TSG101: common types of shorter transcripts are true alternative splice variants
    K U Wagner
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0822, USA
    Oncogene 17:2761-70. 1998
    ..Finally, we examined tsg101 expression patterns during different stages of mammary gland development and in different transgenic mouse models for breast tumorigenesis...
  55. ncbi request reprint Stat5a is mandatory for adult mammary gland development and lactogenesis
    X Liu
    Laboratory of Biochemistry and Metabolism, National Institute of Diabetes and Digestive and Kidney Diseases NIDDK, National Institutes of Health NIH, Bethesda, Maryland 20892 1812, USA
    Genes Dev 11:179-86. 1997
    ..These results document that Stat5a is the principal and an obligate mediator of mammopoietic and lactogenic signaling...
  56. ncbi request reprint Information networks in the mammary gland
    Lothar 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...
  57. ncbi request reprint Deficiency in mouse oxytocin prevents milk ejection, but not fertility or parturition
    W S Young
    Laboratory of Cell Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 4068, USA
    J Neuroendocrinol 8:847-53. 1996
    ..OT injection into the dams restores the milk injection in response to suckling. These results indicate an absolute requirement for oxytocin for successful milk injection, but not for mating, parturition and milk production, in mice...
  58. pmc Loss of cytokine-STAT5 signaling in the CNS and pituitary gland alters energy balance and leads to obesity
    Ji 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...
  59. ncbi request reprint Loss of the peroxisome proliferation-activated receptor gamma (PPARgamma ) does not affect mammary development and propensity for tumor formation but leads to reduced fertility
    Yongzhi 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...
  60. ncbi request reprint 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 I
    Peter 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...
  61. ncbi request reprint The proliferation associated nuclear element (PANE1) is conserved between mammals and fish and preferentially expressed in activated lymphoid cells
    Brian 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...
  62. pmc MMTV-Cre transgenes can adversely affect lactation: considerations for conditional gene deletion in mammary tissue
    Gertraud 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...
  63. pmc Growth hormone-STAT5 regulation of growth, hepatocellular carcinoma, and liver metabolism
    Myunggi 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...
  64. pmc Transcription originating in the long terminal repeats of the endogenous mouse mammary tumor virus MTV-3 is activated in Stat5a-null mice and picks Up hitchhiking exons
    S S Stegalkina
    Laboratory of Genetics and Physiology, National Institute of Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Virol 73:8669-76. 1999
    ..Furthermore, we demonstrate that transcription from the MMTV 5' LTR is highly active in the absence of Stat5a, a transcription factor that had been shown previously to be required for transcription from the MMTV LTR...
  65. ncbi request reprint STAT5A-deficient mice demonstrate a defect in granulocyte-macrophage colony-stimulating factor-induced proliferation and gene expression
    G M Feldman
    Division of Cytokine Biology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892 4555, USA
    Blood 90:1768-76. 1997
    ..These data suggest that the presence of STAT5A during the GM-CSF-induced assembly of STAT5 dimers is critical for the formation of competent transcription factors that are required for both gene expression and cell proliferation...
  66. ncbi request reprint Ectopic TGF beta 1 expression in the secretory mammary epithelium induces early senescence of the epithelial stem cell population
    E C Kordon
    Laboratory of Tumor Immunology and Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 1750
    Dev Biol 168:47-61. 1995
    ....
  67. ncbi request reprint The transcription factor Stat3 is dispensable for pancreatic beta-cell development and function
    Ji 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...
  68. ncbi request reprint Bcl-x is not required for maintenance of follicles and corpus luteum in the postnatal mouse ovary
    Gregory 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...
  69. pmc Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells
    Zhi 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...
  70. pmc Coregulation of Genetic Programs by the Transcription Factors NFIB and STAT5
    Gertraud W Robinson
    Laboratory of Genetics and Physiology G W R, K K, K H Y, Y T, D Y, V C, S J J, L H, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 Department of Microbiology K K, Dankook University, Cheonan 330 714, Republic of Korea Chengdu University of Traditional Chinese Medicine Y T, Chengdu 610072, Republic of China Key Laboratory of Acupuncture and Medicine B M Z, Nanjing University of Traditional Chinese Medicine, Nanjing 210046, Republic of China and New York State Center of Excellence in Bioinformatics and Life Sciences R M G, Department of Biochemistry, Developmental Genomics Group, University at Buffalo, Buffalo, New York 14203
    Mol Endocrinol 28:758-67. 2014
    ..We propose that NFIB-STAT5 modules, possibly in conjunction with other transcription factors, control cell-specific genetic programs. ..
  71. pmc The miR-17/92 cluster is targeted by STAT5 but dispensable for mammary development
    Yonatan 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...
  72. ncbi request reprint RIP-Cre revisited, evidence for impairments of pancreatic beta-cell function
    Ji 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...
  73. ncbi request reprint A morphological and immunohistochemical comparison of mammary tissues from the short-tailed fruit bat (Carollia perspicillata) and the mouse
    Jennifer 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...
  74. ncbi request reprint Differential requirements for shh in mammary tissue and hair follicle morphogenesis
    Marta 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
    ....
  75. ncbi request reprint Transforming growth factor alpha and mouse models of human breast cancer
    R C Humphreys
    National Institutes of Health, National Institute of Digestive, Diabetes and Kidney Disease, Laboratory of Genetics and Physiology, Building 8, Room 111, Bethesda, Maryland, MD 20892, USA
    Oncogene 19:1085-91. 2000
    ..Together these experiments indicate that TGFalpha and the EGFR signaling pathway are potentially amenable to therapies for treatment of human breast disease...
  76. ncbi request reprint An indirect effect of Stat5a in IL-2-induced proliferation: a critical role for Stat5a in IL-2-mediated IL-2 receptor alpha chain induction
    H Nakajima
    Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Immunity 7:691-701. 1997
    ..Correspondingly, we show that Stat5a is essential for maximal responsiveness to antigenic stimuli in vivo, underscoring the physiological importance of IL-2-induced IL-2R alpha expression...
  77. ncbi request reprint Time-sensitive reversal of hyperplasia in transgenic mice expressing SV40 T antigen
    D Ewald
    Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Science 273:1384-6. 1996
    ..These results support a model of time-dependent multistep tumorigenesis, in which virally transformed cells eventually lose their dependence on the viral oncoprotein for maintenance of the transformed state...
  78. ncbi request reprint Conditional deletion of the Bcl-x gene from erythroid cells results in hemolytic anemia and profound splenomegaly
    K U Wagner
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bldg 8, Rm 107, Bethesda, MD 20892 0822, USA
    Development 127:4949-58. 2000
    ..Mice conditionally deficient in Bcl-x permitted us for the first time to study the effects of Bcl-x deficiency on cell proliferation, maturation and survival under physiological conditions in an adult animal...
  79. pmc Loss of STAT1 from mouse mammary epithelium results in an increased Neu-induced tumor burden
    Peter 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...
  80. pmc Activation of beta -catenin signaling in differentiated mammary secretory cells induces transdifferentiation into epidermis and squamous metaplasias
    Keiko 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...
  81. ncbi request reprint Prolactin signaling in mammary gland development
    L Hennighausen
    Laboratory of Biochemistry and Metabolism, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 1812, USA
    J Biol Chem 272:7567-9. 1997
  82. ncbi request reprint Assignment of the murine tumor susceptibility gene 101 (tsg101) and a processed tsg101 pseudogene (tsg101-ps1) to mouse chromosome 7 band B5 and chromosome 15 band D1 by in situ hybridization
    K U Wagner
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive, and Kidney Disease, National Institutes of Health, Bethesda, MD 20892, USA
    Cytogenet Cell Genet 84:87-8. 1999
  83. ncbi request reprint Inhibins and activins regulate mammary epithelial cell differentiation through mesenchymal-epithelial interactions
    G W Robinson
    Laboratory of Metabolism and Biochemistry, NIDDK, National Institutes of Health, Bethesda, MD 20892, USA
    Development 124:2701-8. 1997
    ..The betaB-deficient mice provide the first genetic evidence for stromal signalling in the adult mammary gland in vivo...
  84. ncbi request reprint Signaling pathways in mammary gland development
    L Hennighausen
    Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0822, USA
    Dev Cell 1:467-75. 2001
    ..Here we discuss the signaling pathways that have been adopted by the mammary gland for its own purposes, and the functions they perform...
  85. ncbi request reprint Targeted reduction of oxytocin expression provides insights into its physiological roles
    W S Young
    Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, Maryland, USA
    Adv Exp Med Biol 449:231-40. 1998
    ..These results indicate an absolute requirement for oxytocin for successful milk ejection, but not for mating, parturition and milk production, in mice. Furthermore, homozygous mutant mice show reduced aggression in some tests...
  86. ncbi request reprint Conditional gene expression in secretory tissues and skin of transgenic mice using the MMTV-LTR and the tetracycline responsive system
    L 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...
  87. ncbi request reprint Functional mammary gland development and oncogene-induced tumor formation are not affected by the absence of the retinoblastoma gene
    G W Robinson
    Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, MD 20892, USA
    Oncogene 20:7115-9. 2001
    ....
  88. ncbi request reprint Signal transducer and activator of transcription 5a influences mammary epithelial cell survival and tumorigenesis
    R C Humphreys
    Laboratory of Genetics and Physiology, National Institute of Digestive, Diabetes and Kidney Disease, NIH, Bethesda, Maryland 20892, USA
    Cell Growth Differ 10:685-94. 1999
    ..We also suggest that Stat5a is one of the antecedent, locally acting molecules that initiate the process of epithelial regression and reorganization during involution...
  89. pmc The C/EBPbeta transcription factor regulates epithelial cell proliferation and differentiation in the mammary gland
    G W Robinson
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health NIH, Bethesda, Maryland 20892 1812, USA
    Genes Dev 12:1907-16. 1998
    ..Thus, C/EBPbeta plays an essential, cell autonomous role in the proliferation and differentiation of mammary secretory epithelial cells and is required for the activation of milk protein genes...
  90. ncbi request reprint Bax and Bcl-xs are induced at the onset of apoptosis in involuting mammary epithelial cells
    K Heermeier
    Laboratory of Biochemistry and Metabolism, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1812, USA
    Mech Dev 56:197-207. 1996
    ..These findings point to a significant role for Bax and Bcl-xS in the regulation of apoptosis of secretory alveolar cells during involution...
  91. pmc Signal transducer and activator of transcription (Stat) 5 controls the proliferation and differentiation of mammary alveolar epithelium
    K Miyoshi
    Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Cell Biol 155:531-42. 2001
    ..These data demonstrate that signaling via the PrlR and Stat5 is critical for the proliferation and differentiation of mammary alveoli during pregnancy...
  92. ncbi request reprint Developing a mammary gland is a stat affair
    L Hennighausen
    Laboratory of Biochemistry and Metabolism, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 1812, USA
    J Mammary Gland Biol Neoplasia 2:365-72. 1997
    ..While Stat5 activity has been linked to alveolar proliferation and function, Stat3 activity correlates with the loss of alveolar function, cell death and the initiation of mammary tissue remodeling...
  93. ncbi request reprint Experimental mouse genetics-- answering fundamental questions about mammary gland biology
    J M Shillingford
    Laboratory of Genetics and Physiology, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20817, USA
    Trends Endocrinol Metab 12:402-8. 2001
    ..In addition to these well-established pathways, we address recent data that describe the role of lesser-known genes in the development of the mammary epithelium...
  94. ncbi request reprint The Stat3/5 locus encodes novel endoplasmic reticulum and helicase-like proteins that are preferentially expressed in normal and neoplastic mammary tissue
    Y Cui
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Genomics 78:129-34. 2001
    ..Immunofluorescence studies demonstrated that LGP1 is located in the nuclear envelope and the endoplasmic reticulum. LGP2 is a cytoplasmic protein of 678 amino acids...
  95. pmc Comprehensive meta-analysis of Signal Transducers and Activators of Transcription (STAT) genomic binding patterns discerns cell-specific cis-regulatory modules
    Keunsoo Kang
    Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 8 Center Drive, Bethesda, MD 20892 0822, USA
    BMC Genomics 14:4. 2013
    ..Molecular insight into the biology of STATs was gained from a meta-analysis of 29 available ChIP-seq data sets covering genome-wide occupancy of STATs 1, 3, 4, 5A, 5B and 6 in several cell types...
  96. pmc Genomic dissection of the cytokine-controlled STAT5 signaling network in liver
    Atsushi 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...
  97. ncbi request reprint Conditional mutation of Brca1 in mammary epithelial cells results in blunted ductal morphogenesis and tumour formation
    X Xu
    Genetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Genet 22:37-43. 1999
    ..Our results demonstrate that disruption of Brca1 causes genetic instability and triggers further alterations, including the inactivation of p53, that lead to tumour formation...
  98. ncbi request reprint Bcl-x and Bax regulate mouse primordial germ cell survival and apoptosis during embryogenesis
    E B Rucker
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Mol Endocrinol 14:1038-52. 2000
    ..These findings demonstrate that the balance of Bcl-x and Bax control PGC survival and apoptosis...
  99. pmc Involution of the lactating mammary gland is inhibited by the IGF system in a transgenic mouse model
    S Neuenschwander
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Invest 97:2225-32. 1996
    ..These results demonstrate that IGF-I and IGFBP-3 may modulate the involutionary process of the lactating mammary gland...
  100. ncbi request reprint Validation of transgenic mammary cancer models: goals of the NCI Mouse Models of Human Cancer Consortium and the mammary cancer CD-ROM
    Jeffrey E Green
    Laboratory of Cellular Regulation and Carcinogenesis, National Cancer Institute, Building 41, Bethesda, MD 20892, USA
    Transgenic Res 11:635-6. 2002