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Validated All-in-One™ qPCR Primer for EIF2AK3(NM_004836.6) Search again
Product ID:
HQP022771
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
PEK, PERK, WRS
Gene Description:
eukaryotic translation initiation factor 2 alpha kinase 3
Target Gene Accession:
NM_004836.6(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Gene References into function
- Distinct roles in transcription during the mammalian unfolded protein response.
- Loss of kinase activity in a patient with Wolcott-Rallison syndrome caused by a novel mutation
- PERK plays a role in hypoxia-induced translational attenuation
- results show that PERK binds to and is also inhibited by the hepatitis C virus envelope protein E2
- Genetic heterogeneity between this variant form of WRS and EIF2AK3 WRS correlates with some clinical heterogeneity.
- This pilot study demonstrates an association between the EIF2AK3 gene region and susceptibility to type I diabetes.
- activated by Herpes simplex virus 1 infection
- Inactivation of integrated-stress-response signaling by mutations in the ER kinase PERK and the translation initiation factor eIF2alpha or by a dominant-negative PERK impairs cell survival under extreme hypoxia.
- is the first description of a virus-encoded PERK-specific effector and defines a new strategy by which viruses are able to maintain endoplasmic reticulum homeostasis
- PERK activates glycogen synthase kinase 3 to promote the proteasomal degradation of p53.
- carbon monoxide renders endothelial cells resistant to stress by upregulating Nrf2-dependent HO-1 expression via PERK activation
- PKR and PKR-like endoplasmic reticulum kinase induce the proteasome-dependent degradation of cyclin D1 via a mechanism requiring eukaryotic initiation factor 2alpha phosphorylation
- PERK signaling acts to suppress autophagy and lysosomal dysfunction by increasing the expression of HSP70.
- analysis of endoplasmic reticulum (ER) chaperone regulation and survival of cells compensating for deficiency in the ER stress response kinase, PERK
- The growth-inhibitory function of PERK is preserved in tumors and upon proper reactivation can severely inhibit tumor growth through induction of quiescence.
- PC2, but not pathogenic mutants E837X and R872X, represses cell proliferation through promoting the phosphorylation of eukaryotic translation initiation factor eIF2alpha by pancreatic ER-resident eIF2alpha kinase (PERK).
