transcription factor of the STAT family. Phosphorylated and activated by receptor-associated kinases downstream of certain receptor tyrosine kinases, GPCRs, and receptors for various interleukins and interferons. Forms homo- or heterodimers that translocate into the nucleus where they regulate transcription. Two alternatively spliced isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: DNA-binding; Transcription factor
Cellular Component: nucleoplasm; axon; perinuclear region of cytoplasm; cytoplasm; nuclear chromatin; dendrite; nucleolus; nucleus
Molecular Function: identical protein binding; protein binding; signal transducer activity; enzyme binding; protein homodimerization activity; DNA binding; protein phosphatase 2A binding; sequence-specific DNA binding; double-stranded DNA binding; tumor necrosis factor receptor binding; transcription factor activity; CCR5 chemokine receptor binding
Biological Process: response to peptide hormone stimulus; response to cAMP; blood circulation; positive regulation of transcription, DNA-dependent; positive regulation of smooth muscle cell proliferation; response to lipopolysaccharide; signal transduction; response to exogenous dsRNA; tumor necrosis factor-mediated signaling pathway; regulation of transcription, DNA-dependent; positive regulation of cell proliferation; negative regulation of viral protein levels in host cell; lipopolysaccharide-mediated signaling pathway; response to nutrient; response to drug; caspase activation; transcription, DNA-dependent; cytokine and chemokine mediated signaling pathway; negative regulation of I-kappaB kinase/NF-kappaB cascade; JAK-STAT cascade; negative regulation of angiogenesis; response to bacterium; cellular response to insulin stimulus; response to mechanical stimulus; response to cytokine stimulus; negative regulation of endothelial cell proliferation; positive regulation of transcription from RNA polymerase II promoter
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.