a nuclear protein that may function as a transcriptional repressor. Strongly induced by gamma interferon and, to a lesser extent, by alpha interferon. Binds double-stranded DNA and cell cycle regulatory factors including p53 and Rb. Loss of IFI16 activates p53 checkpoint through NBS1-DNAPK pathway. Inhibits cell growth in the Ras/Raf signaling pathway. May be involved in the senescence of prostate epithelial cells. Expressed in peripheral blood leukocytes, fibroblasts and lymphoid cells. Present in myeloid precursors (CD34+) and throughout monocyte development, but its expression is down-regulated in erythroid and polymorphonuclear precursor cells. Present in prostate, ovary and breast. Four alternatively spliced isoforms have been described. Isoforms-1, -2 and -3 can homo- and hetero-dimerize. Note: This description may include information from UniProtKB.
Molecular Function: protein binding; double-stranded DNA binding; transcription factor binding
Biological Process: positive regulation of cytokine production; transcription, DNA-dependent; monocyte differentiation; response to virus; negative regulation of transcription from RNA polymerase II promoter; negative regulation of DNA binding; cellular response to glucose starvation; cell proliferation; positive regulation of interleukin-1 beta production; negative regulation of viral genome replication; regulation of transcription, DNA-dependent; negative regulation of innate immune response; autophagy; innate immune response; myeloid cell differentiation; regulation of autophagy; positive regulation of transcription from RNA polymerase II promoter; hemopoiesis; negative regulation of transcription, DNA-dependent; inflammatory response; activation of innate immune response; defense response to virus; DNA damage response, signal transduction by p53 class mediator resulting in induction of apoptosis
SS: 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.