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You are here:Home » Antibodies » Abs to Translation Initiation Factors » Anti -EIF2AK2, CT (Eukaryotic Translation Initiation Factor 2-alpha Kinase 2, eIF-2A Protein Kinase 2, Interferon-induced, Double-stranded RNA-activated Protein Kinase, Interferon-inducible RNA-dependent pRotein Kinase, p68 kinase, Protein Kinase RNA-activated,

Anti -EIF2AK2, CT (Eukaryotic Translation Initiation Factor 2-alpha Kinase 2, eIF-2A
Protein Kinase 2, Interferon-induced, Double-stranded RNA-activated Protein Kinase,
Interferon-inducible RNA-dependent pRotein Kinase, p68 kinase, Protein Kinase
RNA-activated,

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Specifications

Clone Host Grade Applications
Polyclonal Rabbit Purified E B IH
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.
Catalog #E8949-16A
ApplicationsSuitable for use in ELISA, Western Blot, and Immunohistochemistry. Other applications not tested.
Recommended DilutionELISA: 1:1,000
Western Blot: 1:100-1:500
Immunohistochemistry: 1:50-1:100
Optimal dilutions to be determined by the researcher.
Storage and StabilityMay be stored at 4°C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
Clone TypePolyclonal
IsotypeIgG
HostRabbit
SourceHuman
ConcentrationAs reported
FormSupplied as a liquid in PBS, 0.09% sodium azide.
PurityPurified by ammonium sulfate precipitation.
ImmunogenSynthetic peptide selected from the C-terminal region of human PRKR (KLH).
SpecificityRecognizes human PRKR. Species Crossreactivity: mouse.
Important NoteThis product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.


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