STAT5B

The protein encoded by this gene is a member of the STAT family of transcription factors. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. This protein mediates the signal transduction triggered by various cell ligands, such as IL2, IL4, CSF1, and different growth hormones. It has been shown to be involved in diverse biological processes, such as TCR signaling, apoptosis, adult mammary gland development, and sexual dimorphism of liver gene expression. This gene was found to fuse to retinoic acid receptor-alpha (RARA) gene in a small subset of acute promyelocytic leukemias (APLL). The dysregulation of the signaling pathways mediated by this protein may be the cause of the APLL.

STAT5B

Carries out a dual function: signal transduction and activation of transcription (PubMed:29844444).
Mediates cellular responses to the cytokine KITLG/SCF and other growth factors. Binds to the GAS element and activates PRL-induced transcription. Positively regulates hematopoietic/erythroid differentiation.

Biological Process activated T cell proliferationIEA:Ensembl
Biological Process B cell differentiationIEA:Ensembl
Biological Process cellular response to epidermal growth factor stimulusISS:UniProtKB
Biological Process cellular response to growth factor stimulusISS:UniProtKB
Biological Process cellular response to hormone stimulusManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process cytokine-mediated signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central
Biological Process defense responseManual Assertion Based On ExperimentIBA:GO_Central
Biological Process development of secondary female sexual characteristicsIEA:Ensembl
Biological Process development of secondary male sexual characteristicsIEA:Ensembl
Biological Process erythrocyte differentiationIEA:Ensembl
Biological Process female pregnancyIEA:Ensembl
Biological Process gamma-delta T cell differentiationIEA:Ensembl
Biological Process growth hormone receptor signaling pathway via JAK-STATManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process lactationIEA:Ensembl
Biological Process lipid storageIEA:Ensembl
Biological Process luteinizationIEA:Ensembl
Biological Process mast cell migrationIEA:Ensembl
Biological Process mitotic cell cycleIEA:Ensembl
Biological Process myeloid cell apoptotic processIEA:Ensembl
Biological Process natural killer cell differentiationIEA:Ensembl
Biological Process natural killer cell mediated cytotoxicityIEA:Ensembl
Biological Process natural killer cell proliferationIEA:Ensembl
Biological Process negative regulation of erythrocyte differentiationIEA:Ensembl
Biological Process negative regulation of myeloid cell apoptotic processIEA:Ensembl
Biological Process Peyer's patch developmentIEA:Ensembl
Biological Process positive regulation of activated T cell proliferationIEA:Ensembl
Biological Process positive regulation of B cell differentiationIEA:Ensembl
Biological Process positive regulation of erythrocyte differentiationManual Assertion Based On ExperimentIDA:UniProtKB
Biological Process positive regulation of gamma-delta T cell differentiationIEA:Ensembl
Biological Process positive regulation of inflammatory responseIEA:Ensembl
Biological Process positive regulation of interleukin-2 productionIEA:Ensembl
Biological Process positive regulation of mitotic cell cycleIEA:Ensembl
Biological Process positive regulation of multicellular organism growthIEA:Ensembl
Biological Process positive regulation of natural killer cell differentiationIEA:Ensembl
Biological Process positive regulation of natural killer cell mediated cytotoxicityIEA:Ensembl
Biological Process positive regulation of natural killer cell proliferationIEA:Ensembl
Biological Process positive regulation of transcription by RNA polymerase IIISS:UniProtKB
Biological Process progesterone metabolic processIEA:Ensembl
Biological Process receptor signaling pathway via JAK-STATManual Assertion Based On ExperimentIBA:GO_Central
Biological Process regulation of cell population proliferationManual Assertion Based On ExperimentIBA:GO_Central
Biological Process regulation of epithelial cell differentiationIEA:Ensembl
Biological Process regulation of multicellular organism growthISS:BHF-UCL
Biological Process regulation of steroid metabolic processIEA:Ensembl
Biological Process regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Biological Process response to estradiolManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process response to interleukin-15IEA:Ensembl
Biological Process response to interleukin-2IEA:Ensembl
Biological Process response to interleukin-4IEA:Ensembl
Biological Process response to peptide hormoneManual Assertion Based On ExperimentIBA:GO_Central
Biological Process T cell differentiation in thymusIEA:Ensembl
Biological Process T cell homeostasisIEA:Ensembl
Biological Process taurine metabolic processISS:BHF-UCL
Biological Process transcription by RNA polymerase IIIEA:Ensembl

Cytoplasm
Nucleus
Translocated into the nucleus in response to phosphorylation.

Growth hormone insensitivity syndrome with immune dysregulation 1, autosomal recessive (GHISID1):
An autosomal recessive form of growth hormone insensitivity syndrome, a congenital disease characterized by short stature, growth hormone deficiency in the presence of normal to elevated circulating concentrations of growth hormone, resistance to exogeneous growth hormone therapy, and recurrent infections. Most, but not all, patients have features of immune dysregulation.
Growth hormone insensitivity syndrome with immune dysregulation 2, autosomal dominant (GHISID2):
An autosomal dominant form of growth hormone insensitivity syndrome, a congenital disease characterized by short stature, growth hormone deficiency in the presence of normal to elevated circulating concentrations of growth hormone, resistance to exogeneous growth hormone therapy, and recurrent infections. GHISID2 patients usually have delayed bone age, delayed puberty, and decreased serum IGF1. Some patients may have features of mild immune dysregulation, such as eczema, increased serum IgE, asthma, or celiac disease.

Tyrosine phosphorylated in response to signaling via activated KIT, resulting in translocation to the nucleus. Tyrosine phosphorylated in response to signaling via activated FLT3; wild-type FLT3 results in much weaker phosphorylation than constitutively activated mutant FLT3. Alternatively, can be phosphorylated by JAK2. Phosphorylation at Tyr-699 by PTK6 or HCK leads to an increase of its transcriptional activity.