產(chǎn)品編號 | bsm-51385M-PE-Cy5.5 |
英文名稱1 | Mouse Anti-EIF2AK3/PERK/PE-Cy5.5 Conjugated antibody |
中文名稱 | PE-Cy5.5標(biāo)記的小鼠抗蛋白激酶樣內(nèi)質(zhì)網(wǎng)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. |
規(guī)格價格 | 100ul/2980元 購買 大包裝/詢價 |
說 明 書 | 100ul |
研究領(lǐng)域 | 免疫學(xué) 染色質(zhì)和核信號 信號轉(zhuǎn)導(dǎo) 新陳代謝 表觀遺傳學(xué) |
抗體來源 | Mouse |
克隆類型 | Monoclonal |
克 隆 號 | 3C3 |
交叉反應(yīng) | (predicted: Human, Mouse, Rat, ) |
產(chǎn)品應(yīng)用 |
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
分 子 量 | 122kDa |
性 狀 | Lyophilized or 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 | Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.05M PB, pH 7.5. |
保存條件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
產(chǎn)品介紹 |
background: 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. Database links: Entrez Gene: 9451 Human Entrez Gene: 13666 Mouse Omim: 604032 Human SwissProt: Q9NZJ5 Human SwissProt: Q9Z2B5 Mouse 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. |