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>   首页   >   产品   >   一抗   >   代谢   >   PERK (EIF2AK3) Antibody (Center)   

PERK (EIF2AK3) Antibody (Center)

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - PERK (EIF2AK3) Antibody (Center) AP8150c
    All lanes : Anti-EIF2AK3 Antibody (Center) at 1:1000 dilution Lane 1: A549 whole cell lysate Lane 2: HepG2 whole cell lysate Lysates/proteins at 20 µg per lane. Secondary Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution. Predicted band size : 125 kDa Blocking/Dilution buffer: 5% NFDM/TBST.
  • 14 - PERK (EIF2AK3) Antibody (Center) AP8150c
    Formalin-fixed and paraffin-embedded human hepatocarcinoma tissue reacted with EIF2AK3 antibody (Center)(Cat.#AP8150c), which was peroxidase-conjugated to the secondary antibody, followed by DAB staining. This data demonstrates the use of this antibody for immunohistochemistry; clinical relevance has not been evaluated.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
IHC-P, WB, E
Primary Accession Q9NZJ5
Other Accession Q9Z1Z1, Q9Z2B5
Reactivity Human
Predicted Mouse, Rat
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 125216 Da
Additional Information
Gene ID 9451
Other Names Eukaryotic translation initiation factor 2-alpha kinase 3, PRKR-like endoplasmic reticulum kinase, Pancreatic eIF2-alpha kinase, HsPEK, EIF2AK3, PEK, PERK
Target/Specificity This PERK antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the Center region of human EIF2AK3.
Dilution IHC-P~~1:100~500
WB~~1:1000
E~~Use at an assay dependent concentration.
Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsPERK (EIF2AK3) Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name EIF2AK3 {ECO:0000303|PubMed:10932183, ECO:0000312|HGNC:HGNC:3255}
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.

BACKGROUND

EIF2AK3, a member of the GCN2 subfamily of Ser/Thr protein kinases, 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. This protein serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin D1. It is proposed that perturbation in protein folding in the endoplasmic reticulum (ER) promotes reversible dissociation from HSPA5/BIP and oligomerization, resulting in transautophosphorylation and kinase activity induction Expression of this Type I membrane protein is ubiquitous, with a high level expression in secretory tissues. Defects in EIF2AK3 are the cause of Wolcott-Rallison syndrome (WRS), 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.

REFERENCES

Delepine, M., et al., Nat. Genet. 25(4):406-409 (2000).
Shi, Y., et al., J. Biol. Chem. 274(9):5723-5730 (1999).
Sood, R., et al., Biochem. J. 346 Pt 2, 281-293 (2000).

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