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首頁>>免疫學>>一抗>>蛋白激酶樣內質網激酶單克隆抗體
蛋白激酶樣內質網激酶單克隆抗體
  • 產品貨號:
    BN42065M
  • 中文名稱:
    蛋白激酶樣內質網激酶單克隆抗體
  • 英文名稱:
    Mouse anti-EIF2AK3/PERK Monoclonal antibody
  • 品牌:
    Biorigin
  • 貨號

    產品規格

    售價

    備注

  • BN42065M-50ul

    50ul

    ¥2020.00

    交叉反應:Human,Mouse(predicted:Rat) 推薦應用:WB,ELISA

  • BN42065M-100ul

    100ul

    ¥3240.00

    交叉反應:Human,Mouse(predicted:Rat) 推薦應用:WB,ELISA

產品描述

英文名稱EIF2AK3/PERK
中文名稱蛋白激酶樣內質網激酶單克隆抗體
別    名DKFZp781H1925; E2AK3_HUMAN; EC 2.7.11.1; EIF2AK3; Eukaryotic translation initiation factor 2 alpha kinase 3; Eukaryotic translation initiation factor 2-alpha kinase 3; Heme regulated EIF2 alpha kinase; HRI; HsPEK; Pancreatic eIF2 alpha kinase; Pancreatic eIF2-alpha kinase; PEK; PRKR like endoplasmic reticulum kinase; PRKR-like endoplasmic reticulum kinase; WRS.  
研究領域免疫學  染色質和核信號  信號轉導  新陳代謝  表觀遺傳學  
抗體來源Mouse
克隆類型Monoclonal
克 隆 號3C3
交叉反應Human, Mouse,  (predicted: Rat, )
產品應用WB=1:200-1000 ELISA=1:5000-10000 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量122kDa
細胞定位細胞漿 
性    狀Liquid
濃    度1mg/ml
免 疫 原Recombinant human EIF2AK3: 
亞    型IgG1
純化方法affinity purified by Protein G
儲 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
PubMedPubMed
產品介紹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. [provided by RefSeq, Jan 2010]

Function:
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. Serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1).

Subunit:
Forms dimers with HSPA5/BIP in resting cells. Oligomerizes in ER-stressed cells. Interacts with DNAJC3.

Subcellular Location:
Endoplasmic reticulum membrane; Single-pass type I membrane protein.

Tissue Specificity:
Ubiquitous. A high level expression is seen in secretory tissues.

Post-translational modifications:
Oligomerization of the N-terminal ER luminal domain by ER stress promotes PERK trans-autophosphorylation of the C-terminal cytoplasmic kinase domain at multiple residues including Thr-982 on the kinase activation loop. Autophosphorylated. Phosphorylated at Tyr-619 following endoplasmic reticulum stress, leading to activate its tyrosine-protein kinase activity. Dephosphorylated by PTPN1/TP1B, leading to inactivate its enzyme activity.
N-glycosylated.
ADP-ribosylated by PARP16 upon ER stress, which increases kinase activity.

DISEASE:
Wolcott-Rallison syndrome (WRS) [MIM:226980]: 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. Note=The disease is caused by mutations affecting the gene represented in this entry.

Similarity:
Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. GCN2 subfamily.
Contains 1 protein kinase domain.

SWISS:
Q9NZJ5

Gene ID:
9451

Database links:

Entrez Gene: 9451 Human

Entrez Gene: 13666 Mouse

Entrez Gene: 29702 Rat

Omim: 604032 Human

SwissProt: Q9NZJ5 Human

SwissProt: Q9Z2B5 Mouse

SwissProt: Q9Z1Z1 Rat

Unigene: 591589 Human

Unigene: 247167 Mouse

Unigene: 24897 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.


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