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SKU:YP-Ab-14182-100UL
PERK Monoclonal Antibody
PERK Monoclonal Antibody
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- Reaction species: Human
- Gene Name: EIF2AK3
- Protein name: Eukaryotic translation initiation factor 2-alpha kinase 3
- Molecular weight (DA): 125kD
- Immunogen: Purified recombinant fragment of human PERK expressed in E. Coli.
- Specificity: PERK Monoclonal Antibody detects endogenous levels of PERK protein.
- Composition: Ascitic fluid containing 0.03% sodium azide,0.5% BSA, 50%glycerol.
- Source: Monoclonal, Mouse
- Dilution ratio: Western Blot: 1/500 - 1/2000. ELISA: 1/10000. Not yet tested in other applications.
- Purification process: Affinity purification
- Storage: -20°C/1 year
- Other Names: EIF2AK3; PEK; PERK; Eukaryotic translation initiation factor 2-alpha kinase 3; PRKR-like endoplasmic reticulum kinase; Pancreatic eIF2-alpha kinase; HsPEK
- Background: The protein encoded by this gene phosphorylates the alpha subunit of eukaryotic translation-initiation factor 2, leading to its inactivation, and thus to a rapid reduction of translational initiation and repression of global protein synthesis. This protein is thought to modulate mitochondrial function. It is a type I membrane protein located in the endoplasmic reticulum (ER), where it is induced by ER stress caused by malfolded proteins. Mutations in this gene are associated with Wolcott-Rallison syndrome. [provided by RefSeq, Sep 2015],
- Function: catalytic activity:ATP + a protein = ADP + a phosphoprotein.,disease:Defects in EIF2AK3 are the cause of Wolcott-Rallison syndrome (WRS) [MIM:226980]; also known as multiple epiphyseal dysplasia with early-onset diabetes mellitus. WRS is a rare autosomal recessive disorder, characterized by permanent neonatal or early infancy insulin-dependent diabetes and, at a later age, epiphyseal dysplasia, osteoporosis, growth retardation and other multisystem manifestations, such as hepatic and renal dysfunctions, mental retardation and cardiovascular abnormalities.,domain:The lumenal domain senses perturbations in protein folding in the ER, probably through reversible interaction with HSPA5/BIP.,enzyme regulation:Perturbation in protein folding in the endoplasmic reticulum (ER) promotes reversible dissociation from HSPA5/BIP and oligomerization, resulting in transautophosphorylation and kinase act
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