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PKR (PRKR) Antibody (N-term Y27) Blocking peptide



  • Format: Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed.
  • Gene Id: 5610
  • Category: Peptides; Blocking Peptides
  • Subtitle: Synthetic peptide
  • Gene Name: EIF2AK2
  • Other Names: Interferon-induced, double-stranded RNA-activated protein kinase, Eukaryotic translation initiation factor 2-alpha kinase 2, eIF-2A protein kinase 2, Interferon-inducible RNA-dependent protein kinase, P1/eIF-2A protein kinase, Protein kinase RNA-activated, PKR, Protein kinase R, Tyrosine-protein kinase EIF2AK2, p68 kinase, EIF2AK2, PKR, PRKR
  • Availability: 2 weeks
  • Bio Background: Interferon-induced, double-stranded RNA-activated protein kinase (PRKR) is a serine-threonine kinase. Activation by dsRNAs leads to autophosphorylation of PRKR and allows the kinase to phosphorylate its natural substrate, the alpha subunit of eukaryotic protein synthesis initiation factor-2 (EIF2-alpha), leading to the inhibition of protein synthesis. Human gamma-interferon (IFNG) mRNA exploits localized activation of PRKR in the cell to regulate its own translation. IFNG mRNA activates PRKR through a pseudoknot in its 5-prime untranslated region. The HCV envelope protein E2 contains a sequence identical with phosphorylation sites of the interferon-inducible protein kinase PRKR and the translation initiation factor EIF2-alpha, a target of PRKR. E2 inhibits the kinase activity of PRKR and blocks its inhibitory effect on protein synthesis and cell growth, which provides one mechanism by which HCV may circumvent the antiviral effect of interferon. PRKR, which is involved in TLR signaling and mediates apoptosis in fibroblasts in response to viral infection and inflammatory cytokines, also activates IKK and NFKB, thereby suppressing apoptosis. Apoptosis induced by live pathogenic gram-positive and gram-negative bacteria requirs both TLR4 and PRKR, possibly representing a major mechanism for pathogenic bacteria that use specific virulence factors to avoid detection and destruction by the innate immune system. Roles for PRKR activation in Huntington disease and Fanconi anemia have also been suggested.
  • Bio References: Beisser, P.S., et al., J. Virol. 79(1):441-449 (2005).Gerotto, M., et al., Antivir. Ther. (Lond.) 9(5):763-770 (2004).Zhang, X., et al., J. Biol. Chem. 279(42):43910-43919 (2004).Gil, J., et al., Mol. Cell. Biol. 24(10):4502-4512 (2004).Hii, S.I., et al., Int. J. Cancer 109(3):329-335 (2004).
  • Other Accession: Q52M43
  • Primary Accession: P19525
  • Targetspecificity: The synthetic peptide sequence used to generate the antibody AP8151c was selected from the N-term region of human PRKR-Y27. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.