a protein kinase of the PEK family. Upon binding double-stranded RNA, it becomes autophosphorylated and activated. Phosphorylates and inhibits the alpha subunit of eIF2 alpha, which leads to an inhibition of the initiation of protein synthesis. Controls the activation of several transcription factors such as NF-kappaB, p53 and Stats. Mediates apoptosis induced by many different stimuli, such as LPS, TNF-alpha, viral infection and serum starvation. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; Translation; EC 18.104.22.168; Protein kinase, Other; EC 22.214.171.124; Protein kinase, Ser/Thr (non-receptor); Other group; PEK family
Cellular Component: membrane; perinuclear region of cytoplasm; cytoplasm; nucleus; cytosol
Molecular Function: protein serine/threonine kinase activity; protein binding; double-stranded RNA binding; non-membrane spanning protein tyrosine kinase activity; protein phosphatase type 2A regulator activity; eukaryotic translation initiation factor 2alpha kinase activity; ATP binding; protein kinase activity
Biological Process: positive regulation of cytokine production; peptidyl-tyrosine phosphorylation; activation of MAPKK activity; transcription, DNA-dependent; translation; unfolded protein response; response to virus; protein amino acid autophosphorylation; viral infectious cycle; protein amino acid phosphorylation; evasion by virus of host immune response; positive regulation of stress-activated MAPK cascade; positive regulation of chemokine production; activation of NF-kappaB transcription factor; negative regulation of cell proliferation; modification by virus of host cellular process; negative regulation of viral genome replication; virus-host interaction; negative regulation of translation; innate immune response; negative regulation of osteoblast proliferation; defense response to virus
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.