PKR is a 68 kDa protein and an IFN-induced serine/threonine protein kinase consisting of two N-terminal RNA-binding regulatory domains and a functional C-terminal serine/threonine protein kinase domain. Activated by dsRNA produced during viral infections, PKR plays a key role in IFN induced-innate antiviral response, virus-induced apoptosis, cell growth & differentiation. Upon activation, PKR gets autophosphorylated and catalyzes the phosphorylation of elF2 alpha subunit, which leads to an inhibition of protein synthesis. PKR induces apoptosis by up-regulating Fas expression and mediates FADD/Caspase-8 death signaling pathway. Upon viral infection, it functions as a dual protein, sequentially activating both cell survival & cell death pathways using kinase independent and dependent strategies. PRKR regulates multiple pathways which include NF-kappaB activation, p53, p38, & PDGF signaling pathway. PKR has been implicated in tumor suppression & malignancy. To evade the antiviral effects of PKR, viruses have evolved multiple mechanisms, such as the inhibition of PKR by the non-structural protein (NS1) of the influenza virus. More recently, PKR has been implicated in several neurodegenerative diseases including Alzheimer, Huntington, and amyotrophic lateral sclerosis.
Clicking the images or links will redirect you to a website hosted by BenchSci that provides third-party
scientific content. Neither the content nor the BenchSci technology and processes for
selection have been evaluated by us; we are providing them as-is and without warranty of any kind,
including for use or application of the Thermo Fisher Scientific products presented.