PKR (EIF2AK2) (N-term) Rabbit Polyclonal Antibody

Specifications

Product Data
Applications	IHC, WB
Recommend Dilution	ELISA: 1/1,000. Western blotting: 1/100 - 1/500. Immunohistochemistry: 1/50 - 1/100. Flow cytometry.
Reactivity	Human, Mouse
Host	Rabbit
Clonality	Polyclonal
Immunogen	This antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the N-terminal region of human PRKR.
Specificity	This antibody reacts to PRKR.
Formulation	PBS with 0.09% (W/V) sodium azide State: Purified State: Liquid purified Ig
Concentration	lot specific
Purification	Prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS
Conjugation	Unconjugated
Storage Condition	Store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing.
Gene Name	eukaryotic translation initiation factor 2 alpha kinase 2
Database Link	Entrez Gene 5610 Human UniProt ID P19525
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.
Synonyms	eIF-2A protein kinase 2, PRKR
Reference Data

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