ISR-alpha 抗体 (AA 701-760)
(1 reference)-
- 抗原 See all ISR-alpha 抗体
- ISR-alpha (Insulin Receptor alpha (ISR-alpha))
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抗原表位
- AA 701-760
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适用
- 人, 大鼠
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宿主
- 兔
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克隆类型
- 多克隆
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标记
- This ISR-alpha antibody is un-conjugated
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应用范围
- Immunofluorescence (Cultured Cells) (IF (cc)), Immunofluorescence (Paraffin-embedded Sections) (IF (p)), Western Blotting (WB), Flow Cytometry (FACS), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), ELISA, Immunohistochemistry (Frozen Sections) (IHC (fro))
- 交叉反应
- 人, 大鼠
- 预测反应
- Mouse,Dog,Cow,Sheep,Pig,Horse,Chicken,Rabbit
- 纯化方法
- Purified by Protein A.
- 免疫原
- KLH conjugated synthetic peptide derived from human Insulin Receptor alpha
- 亚型
- IgG
- Top Product
- Discover our top product ISR-alpha Primary Antibody
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anti-Insulin Receptor alpha (ISR-alpha) antibody
ISR-alpha 适用: 人, 大鼠, 小鼠 IF, IHC 宿主: 兔 Polyclonal unconjugated
anti-Insulin Receptor alpha (ISR-alpha) (AA 51-150) antibodyISR-alpha 适用: 人, 大鼠 IF (cc), IF (p), IHC (p), ELISA, IHC (fro) 宿主: 兔 Polyclonal unconjugated
anti-Insulin Receptor alpha (ISR-alpha) antibodyISR-alpha 适用: 人 Crys 宿主: 兔 Chimeric Fab 83-7 unconjugated Recombinant Antibody
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- 应用备注
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WB 1:300-5000
ELISA 1:500-1000
FCM 1:20-100
IHC-P 1:200-400
IHC-F 1:100-500
IF(IHC-P) 1:50-200
IF(IHC-F) 1:50-200
IF(ICC) 1:50-200 - 限制
- 仅限研究用
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- 状态
- Liquid
- 浓度
- 1 μg/μL
- 缓冲液
- 0.01M TBS( pH 7.4) with 1 % BSA, 0.02 % Proclin300 and 50 % Glycerol.
- 储存液
- ProClin
- 注意事项
- This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.
- 储存条件
- 4 °C,-20 °C
- 储存方法
- Shipped at 4°C. Store at -20°C for one year. Avoid repeated freeze/thaw cycles.
- 有效期
- 12 months
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: "APT070 (mirococept), a membrane-localizing C3 convertase inhibitor, attenuates early human islet allograft damage in vitro and in vivo in a humanized mouse model." in: British journal of pharmacology, Vol. 173, Issue 3, pp. 575-87, (2016) (PubMed).
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: "APT070 (mirococept), a membrane-localizing C3 convertase inhibitor, attenuates early human islet allograft damage in vitro and in vivo in a humanized mouse model." in: British journal of pharmacology, Vol. 173, Issue 3, pp. 575-87, (2016) (PubMed).
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- 抗原
- ISR-alpha (Insulin Receptor alpha (ISR-alpha))
- 别名
- Insulin Receptor alpha (ISR-alpha 产品)
- 别名
- CD220 antibody, HHF5 antibody, insulin receptor antibody, INSR antibody
- 背景
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Synonyms: HHF5, CD220, Insulin receptor, IR, INSR, Insulin receptor subunit alpha, PRO_0000016687
Background: Receptor tyrosine kinase which mediates the pleiotropic actions of insulin. Binding of insulin leads to phosphorylation of several intracellular substrates, including, insulin receptor substrates (IRS1, 2, 3, 4), SHC, GAB1, CBL and other signaling intermediates. Each of these phosphorylated proteins serve as docking proteins for other signaling proteins that contain Src-homology-2 domains (SH2 domain) that specifically recognize different phosphotyrosines residues, including the p85 regulatory subunit of PI3K and SHP2. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway, which is responsible for most of the metabolic actions of insulin, and the Ras-MAPK pathway, which regulates expression of some genes and cooperates with the PI3K pathway to control cell growth and differentiation. Binding of the SH2 domains of PI3K to phosphotyrosines on IRS1 leads to the activation of PI3K and the generation of phosphatidylinositol-(3, 4, 5)-triphosphate (PIP3), a lipid second messenger, which activates several PIP3-dependent serine/threonine kinases, such as PDPK1 and subsequently AKT/PKB. The net effect of this pathway is to produce a translocation of the glucose transporter SLC2A4/GLUT4 from cytoplasmic vesicles to the cell membrane to facilitate glucose transport. Moreover, upon insulin stimulation, activated AKT/PKB is responsible for: anti-apoptotic effect of insulin by inducing phosphorylation of BAD, regulates the expression of gluconeogenic and lipogenic enzymes by controlling the activity of the winged helix or forkhead (FOX) class of transcription factors. Another pathway regulated by PI3K-AKT/PKB activation is mTORC1 signaling pathway which regulates cell growth and metabolism and integrates signals from insulin. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway.
- 基因ID
- 3643
- UniProt
- P06213
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