STAT5 Transcription Factor

• 

  Subject Areas on Research

  • A human erythropoietin receptor gene mutant causing familial erythrocytosis is associated with deregulation of the rates of Jak2 and Stat5 inactivation. 
  • ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling. 
  • Akt is required for Stat5 activation and mammary differentiation. 
  • Autocrine prolactin induced by the Pten-Akt pathway is required for lactation initiation and provides a direct link between the Akt and Stat5 pathways. 
  • DNA-remethylation around a STAT5-binding enhancer in the alphaS1-casein promoter is associated with abrupt shutdown of alphaS1-casein synthesis during acute mastitis. 
  • Differential and complementary effects of glucose and prolactin on islet DNA synthesis and gene expression. 
  • Erythropoietin hypersensitivity in primary familial and congenital polycythemia: role of tyrosines Y285 and Y344 in erythropoietin receptor cytoplasmic domain. 
  • Familial polycythemia due to truncations of the erythropoietin receptor. 
  • Fatty acid transport protein 2 reprograms neutrophils in cancer. 
  • Genome-wide analysis of STAT target genes: elucidating the mechanism of STAT-mediated oncogenesis. 
  • Growth hormone and prolactin receptors in adipogenesis: STAT-5 activation, suppressors of cytokine signaling, and regulation of insulin-like growth factor I. 
  • Hematopoietic-specific Stat5-null mice display microcytic hypochromic anemia associated with reduced transferrin receptor gene expression. 
  • Human immunodeficiency virus type 1 (HIV-1) induces activation of multiple STATs in CD4+ cells of lymphocyte or monocyte/macrophage lineages. 
  • Hydrophobic residues Phe751 and Leu753 are essential for STAT5 transcriptional activity. 
  • IL-7 promotes Glut1 trafficking and glucose uptake via STAT5-mediated activation of Akt to support T-cell survival. 
  • Interleukin-3-induced activation of the JAK/STAT pathway is prolonged by proteasome inhibitors. 
  • Isolation of unique STAT5 targets by chromatin immunoprecipitation-based gene identification. 
  • JAK-STAT and G-protein-coupled receptor signaling pathways are frequently altered in epitheliotropic intestinal T-cell lymphoma. 
  • JAK2 is required for induction of the murine DUB-1 gene. 
  • Janus kinase 3 (JAK3) deficiency: clinical, immunologic, and molecular analyses of 10 patients and outcomes of stem cell transplantation. 
  • Janus kinase 3-activating mutations identified in natural killer/T-cell lymphoma. 
  • Loss of Nuclear Localized Parathyroid Hormone-Related Protein in Primary Breast Cancer Predicts Poor Clinical Outcome and Correlates with Suppressed Stat5 Signaling. 
  • Loss of beta-catenin impairs the renewal of normal and CML stem cells in vivo. 
  • Loss of nuclear localized and tyrosine phosphorylated Stat5 in breast cancer predicts poor clinical outcome and increased risk of antiestrogen therapy failure. 
  • Non-erythroid effects of erythropoietin. 
  • Prolactin can modulate CD4+ T-cell response through receptor-mediated alterations in the expression of T-bet. 
  • Prolactin induction of insulin gene transcription: roles of glucose and signal transducer and activator of transcription 5. 
  • Receptors that induce erythroid differentiation of Ba/F3 cells: structural requirements and effect on STAT5 binding. 
  • TNK1 is a ubiquitin-binding and 14-3-3-regulated kinase that can be targeted to block tumor growth. 
  • The interplay of prolactin and the glucocorticoids in the regulation of beta-cell gene expression, fatty acid oxidation, and glucose-stimulated insulin secretion: implications for carbohydrate metabolism in pregnancy. 
  • Transcriptional Profiling of CD8+ CMV-Specific T Cell Functional Subsets Obtained Using a Modified Method for Isolating High-Quality RNA From Fixed and Permeabilized Cells. 
  • Transient CD86 expression on hepatitis C virus-specific CD8+ T cells in acute infection is linked to sufficient IL-2 signaling. 
• 

  Keywords of People

  • Freemark, Michael Scott, Robert C. Atkins, M.D. and Veronica Atkins Distinguished Professor of Pediatrics, in the School of Medicine, Pediatrics, Endocrinology