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Symbol STAT5B contributors: mct/npt - updated : 24-02-2018
HGNC name signal transducer and activator of transcription 5B
HGNC id 11367
Corresponding disease
GHIS3 growth hormone insensitivity 3
Location 17q21.2      Physical location : 40.351.195 - 40.428.424
Synonym name transcription factor STAT5B
Synonym symbol(s) STAT5
TYPE functioning gene
STRUCTURE 77.23 kb     19 Exon(s)
10 Kb 5' upstream gene genomic sequence study
regulatory sequence alternative promoter
text structure an alternative tissue specific promoter
MAPPING cloned Y linked N status provisional
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
19 - 5171 - 787 - Lin (1996)
Type ubiquitous
   expressed in (based on citations)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Endocrineneuroendocrinepituitary  highly
Lymphoid/Immunelymph node   highly
 thymus   highly
Reproductivemale systemtestis   
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Blood / Hematopoieticbone marrow   
SystemCellPubmedSpeciesStageRna symbol
cell lineage
cell lines
fluid/secretion lymph
  • a N terminus conserved domain,the coiled coil domain,
  • the DNA binding domain,a linker region,
  • a SRC homology domain 2 (SH2), a critical site of tyrosine phosphorylation
  • the carboxy-terminal transactivation domain
  • mono polymer homomer , heteromer , dimer
  • STAT family of transcription factors
  • CATEGORY immunity/defense , transcription factor
    SUBCELLULAR LOCALIZATION     intracellular
    text translocated into the nucleus in response to phosphorylation
    basic FUNCTION
  • regulator of transcription having a dual function: signal transduction and activation of transcription
  • functioning to transduce signals from cytokines to the nucleus where it regulates gene expression
  • playing a crucial role in mammary epithelium displaying reciprocal activation kinetics during pregnancy, lactation and involution
  • signal transducer and activator of transcription 5A and 5B (STAT5A/B) is critical for the viability of prostate cancer cells (Tan 2008)
  • potential role of the STAT5B-RUNX interaction in lymphocyte development
  • STAT5A/B directs GM-CSF signaling through the regulation of proliferation and survival genes (Kimura 2009)
  • critical role of STAT5A, STAT5B transcription factor tetramerization for cytokine responses and normal immune function
  • STAT5B and STAT5A act partly as non-redundant transcription factors and that STAT5B is more critical for Treg maintenance and function in humans
  • CELLULAR PROCESS nucleotide, transcription, regulation
    text immune response
    signaling signal transduction
    a component
  • homodimerizing or heterodimerizing with STAT5A
  • PLCB3 form the multimolecular SPS complex together with PTPN6 and STAT5
    small molecule
  • binds to the NCAM2 intron in the NKL natural killer cell line (this binding is induced by cytokines that activate STAT5B)
  • physically interacts with RUNX1, RUNX2 and RUNX3
  • BCL10 is an IL2-independent STAT5B target gene
  • SLC30A2 participates in zinc transport into pancreatic zymogen granules through a glucocorticoid pathway requiring glucocorticoid receptor and STAT5, and zinc-regulated signaling pathways requiring MTF1
  • functions for GAB2 in hematopoiesis in a manner that is non-redundant with STAT5B
  • LYN/PLCB3-mediated regulatory mechanism of PTPN6 and STAT5B activities
  • DUSP4 suppresses CD4(+) T-cell proliferation through novel regulations in STAT5B phosphorylation and IL2 signaling
  • key regulator of lymphoid development, that is modified by SUMO-2 and is specifically regulated by SENP1
  • crucial role of SENP1 in the regulation of STAT5B activation during early lymphoid development
  • elevated SKIL promotes STAT5B signaling by enhancing its stability, thereby sharply increasing the activity of prolactin signaling at the onset of lactation
  • STAT5B, but not STAT5A, was upregulated in PDZRN3-depleted cells at both mRNA and protein levels
  • STAT3 increases expression of BCL6 and enhances recruitment of RNA polymerase II phosphorylated at a site associated with transcriptional initiation, but STAT5B represses BCL6 expression below basal levels and decreases the association of RNA polymerase II at the gene
  • SIRT1 negatively regulates GH-induced STAT5A, STAT5B phosphorylation and IGF1 production via deacetylation of STAT5A, STAT5B in the liver
  • SIRT1 deacetylates STAT5B by direct interaction
  • NFIB-STAT5 modules, possibly in conjunction with other transcription factors, control cell-specific genetic programs
  • STAT5B transcription factor directly bound to the promoter and an intronic region of the GATA2 gene, and the STAT5B-GATA2 pathway is critical for basophil and mast cell differentiation and maintenance
  • control of CD8 T cell proliferation and terminal differentiation by active STAT5B and CDKN2A/CDKN2B
  • DUSP4 regulates STAT5B protein stability and helper T cell polarization
  • STAT5B was the target of GRAMD1A, GRAMD1A regulated the target genes of STAT5B and the transcriptional activity of STAT5B
  • RGS4 is implicated in opioid dependent neuronal differentiation and neurite outgrowth via a "non-canonical" signaling pathway regulating STAT5B-directed responses
  • BRD9-STAT5 axis as critical for leukemia maintenance
  • cell & other
  • T cell receptor and stimulating T cell proliferation
    activated by interleukin 2 and other cytokines
    GH, strongly activated by prolactin (PRL) towards the end of pregnancy, persists in an activated state during lactation, and is rapidly inactivated after cessation of suckling
    repressed by NCOR2
    Other its signaling can be modulated by its coupling with a specific subset of G protein subunits, revealing a novel signaling mechanism for the transcriptional regulation of STAT5B-dependent genes (Georganta 2010)
    regulated by SRC (SRC may regulate STAT5B in the intracellular signalling pathway important for the proliferation of normal human B lymphocytes)(Cayer 2009)
    corresponding disease(s) GHIS3
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral fusion      
    with RARA, 5' - STAT5B - RARA - 3', in a small subset of acute promyelocytic leukemias
    Variant & Polymorphism
    Candidate gene
    Therapy target
    inhibitors that disrupt STAT5B function independent of tyrosine phosphorylation may be therapeutically effective in treating certain leukemias/lymphomas