EIF2AK3 Antibody
Purified Mouse Monoclonal Antibody
- 产品详情
- 实验流程
Application ![]()
| WB, E |
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Primary Accession | Q9NZJ5 |
Reactivity | Human |
Host | Mouse |
Clonality | Monoclonal |
Clone Names | 5G5 |
Isotype | IgG1 |
Calculated MW | 125216 Da |
Description | The protein encoded by this gene phosphorylates the alpha subunit of eukaryotic translation-initiation factor 2 (EIF2), leading to its inactivation, and thus to a rapid reduction of translational initiation and repression of global protein synthesis. 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. |
Immunogen | Purified recombinant fragment of human EIF2AK3 expressed in E. Coli. |
Formulation | Ascitic fluid containing 0.03% sodium azide. |
Gene ID | 9451 |
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Other Names | Eukaryotic translation initiation factor 2-alpha kinase 3, 2.7.11.1, PRKR-like endoplasmic reticulum kinase, Pancreatic eIF2-alpha kinase, HsPEK, EIF2AK3, PEK, PERK |
Dilution | WB~~1/500 - 1/2000 E~~N/A |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | EIF2AK3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | EIF2AK3 {ECO:0000303|PubMed:10932183, ECO:0000312|HGNC:HGNC:3255} |
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Function | Metabolic-stress sensing protein kinase that phosphorylates the alpha subunit of eukaryotic translation initiation factor 2 (EIF2S1/eIF-2-alpha) in response to various stress, such as unfolded protein response (UPR) (PubMed:10026192, PubMed:10677345, PubMed:11907036, PubMed:12086964, PubMed:25925385, PubMed:31023583). Key effector of the integrated stress response (ISR) to unfolded proteins: EIF2AK3/PERK specifically recognizes and binds misfolded proteins, leading to its activation and EIF2S1/eIF-2-alpha phosphorylation (PubMed:10677345, PubMed:27917829, PubMed:31023583). EIF2S1/eIF-2-alpha phosphorylation in response to stress converts EIF2S1/eIF-2-alpha in a global protein synthesis inhibitor, leading to a global attenuation of cap-dependent translation, while concomitantly initiating the preferential translation of ISR-specific mRNAs, such as the transcriptional activators ATF4 and QRICH1, and hence allowing ATF4- and QRICH1-mediated reprogramming (PubMed:10026192, PubMed:10677345, PubMed:31023583, PubMed:33384352). The EIF2AK3/PERK- mediated unfolded protein response increases mitochondrial oxidative phosphorylation by promoting ATF4-mediated expression of COX7A2L/SCAF1, thereby increasing formation of respiratory chain supercomplexes (PubMed:31023583). In contrast to most subcellular compartments, mitochondria are protected from the EIF2AK3/PERK-mediated unfolded protein response due to EIF2AK3/PERK inhibition by ATAD3A at mitochondria-endoplasmic reticulum contact sites (PubMed:39116259). In addition to EIF2S1/eIF-2-alpha, also phosphorylates NFE2L2/NRF2 in response to stress, promoting release of NFE2L2/NRF2 from the BCR(KEAP1) complex, leading to nuclear accumulation and activation of NFE2L2/NRF2 (By similarity). Serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1) (By similarity). Involved in control of mitochondrial morphology and function (By similarity). |
Cellular Location | Endoplasmic reticulum membrane {ECO:0000250|UniProtKB:Q9Z2B5}; Single-pass type I membrane protein. Note=Localizes to the Localizes to endoplasmic reticulum membrane (By similarity). Also present at mitochondria-endoplasmic reticulum contact sites; where it interacts with ATAD3A (PubMed:39116259). {ECO:0000250|UniProtKB:Q9Z2B5, ECO:0000269|PubMed:39116259} |
Tissue Location | Ubiquitous. A high level expression is seen in secretory tissues. |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
REFERENCES
1. Autophagy. 2008 Apr 1;4(3):364-7. 2. J Biol Chem. 2008 Jun 20;283(25):17020-9. 3. Hum Mol Genet. 2008 Oct 15;17(20):3254-62.

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