|Tested species reactivity||Human, Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Peptide sequence around phosphorylation site of threonine 446 (K-R-T(p)-R-S) derived from Human PKR.|
|Storage buffer||PBS, pH 7.4, with 50% glycerol, 150mM NaCl|
|Contains||0.02% sodium azide|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:50-1:100|
|Western Blot (WB)||1:500-1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
A suggested positive control for Western blot is K562 cells; suggested positive control for IHC is human colon carcinoma; suggested positive control for ICC/IF is Hela cells.
PRKR, a 68KDa protein, is 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, it plays a key role in IFN induced-innate antiviral response, virus-induced apoptosis, cell growth and differentiation. Upon activation, PRKR gets autophosphorylated and catalyzes the phosphorylation of elF2 alpha subunit, which leads to an inhibition of protein synthesis. It 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 and cell death pathways using kinase independent and dependent strategies. PRKR regulates multiple pathways which include NF-kappaB activation, p53, p38, and PDGF signaling pathway. Its role has been implicated in tumor suppression and malignancy.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.