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: axon; cytoplasm; dendrite; nuclear chromatin; nucleolus; nucleoplasm; nucleus; perinuclear region of cytoplasm
Molecular Function: CCR5 chemokine receptor binding; DNA binding; double-stranded DNA binding; enzyme binding; identical protein binding; protein binding; protein homodimerization activity; protein phosphatase 2A binding; sequence-specific DNA binding; signal transducer activity; transcription factor activity; tumor necrosis factor receptor binding
Biological Process: blood circulation; caspase activation; cellular response to insulin stimulus; cytokine and chemokine mediated signaling pathway; JAK-STAT cascade; lipopolysaccharide-mediated signaling pathway; negative regulation of angiogenesis; negative regulation of endothelial cell proliferation; negative regulation of I-kappaB kinase/NF-kappaB cascade; negative regulation of viral protein levels in host cell; positive regulation of cell proliferation; positive regulation of smooth muscle cell proliferation; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; regulation of transcription, DNA-dependent; response to bacterium; response to cAMP; response to cytokine stimulus; response to drug; response to exogenous dsRNA; response to lipopolysaccharide; response to mechanical stimulus; response to nutrient; response to peptide hormone stimulus; signal transduction; transcription, DNA-dependent; tumor necrosis factor-mediated signaling pathway
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.