推荐产品
生物来源
mouse
质量水平
抗体形式
purified antibody
抗体产品类型
primary antibodies
克隆
24.6.2, monoclonal
种属反应性
bovine, pig, mouse, monkey, canine, rat, human
技术
immunocytochemistry: suitable
immunofluorescence: suitable
immunoprecipitation (IP): suitable
western blot: suitable
同位素/亚型
IgG2aκ
NCBI登记号
UniProt登记号
运输
wet ice
靶向翻译后修饰
phosphorylation (pSer307 )
基因信息
bovine ... Irs1(538598)
dog ... Irs1(486148)
human ... IRS1(3667)
mouse ... Irs1(16367)
pig ... Irs1(100512686)
rat ... Irs1(25467)
rhesus monkey ... Irs1(707870)
一般描述
IRS1 (Insulin Receptor Substrate 1) transmits insulin signals via metabolic and mitogenic pathways. IRS1 is heavily phosphorylated on both serine and tyrosine residues. These phosphorylated tyrosines enable IRS to act as a docking protein that binds SH2 domains of such proteins as PI3 Kinase (phosphatidylinositol 3-kinase) and GRB2, resulting in activation. Over expression and phosphorylation of serine is associated with insulin resistance and breast cancer. Some of the more notable phosphorylation sites are Ser302 that is phosphorylated following insulin stimulation. Ser307, phosphorylated by JNK and IKK, is a key regulatory site that appears to disrupt the IRS1/IR interaction and inhibits insulin-mediated activation of the PI3 kinase and MAPK pathways, and Ser636/639 that is known to be phosphorylated by p70S6K downstream of mTOR and acts as a negative feedback loop.
特异性
Predicted to cross-react with many other species based on 100% sequence homology with immunogen.
This antibody recognizes IRS1 phosphorylated at Ser307 (mouse) and Ser312 (human).
免疫原
Synthetic peptide corresponding to amino acids surrounding phosphorylated Ser307 of mouse IRS1.
应用
This Anti-phospho-IRS1 (Ser307 mouse/ Ser312 human) Antibody, clone 24.6.2 is validated for use in WB, IP, IC, IF for the detection of phospho-IRS1 (Ser307 mouse/ Ser312 human).
质量
Evaluated by western blot on IR/IRS1 transfected CHO +/- Insulin lysate.
Western Blot Analysis:
1:1,000 dilution of this antibody was used to detect IRS1 in IRS/IR transfected CHO -/+ Calyculin A/ Okadaic Acid-treated cell lysate.
Western Blot Analysis:
1:1,000 dilution of this antibody was used to detect IRS1 in IRS/IR transfected CHO -/+ Calyculin A/ Okadaic Acid-treated cell lysate.
目标描述
~185 kDa
联系
Replaces: 07-247
外形
Format: Purified
其他说明
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Xinghui Sun et al.
Circulation research, 118(5), 810-821 (2016-02-03)
The pathogenesis of insulin resistance involves dysregulated gene expression and function in multiple cell types, including endothelial cells (ECs). Post-transcriptional mechanisms such as microRNA-mediated regulation of gene expression could affect insulin action by modulating EC function. To determine whether microRNA-181b
Hua Yan et al.
Molecular medicine reports, 15(1), 180-186 (2016-12-03)
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, the pathological process of which is complex. Activation of the c‑Jun N‑terminal kinase (JNK) signaling pathway is associated with the mechanism underlying obesity-induced insulin resistance. Furthermore, the JNK signaling
Ashraf Nahle et al.
International journal of molecular sciences, 22(24) (2021-12-25)
The NAD-dependent deacetylase SIRT1 improves β cell function. Accordingly, nicotinamide mononucleotide (NMN), the product of the rate-limiting step in NAD synthesis, prevents β cell dysfunction and glucose intolerance in mice fed a high-fat diet. The current study was performed to
Saori Kakehi et al.
Frontiers in physiology, 14, 1198390-1198390 (2023-06-30)
Inactivity causes insulin resistance in skeletal muscle and exacerbates various lifestyle-related diseases. We previously found that 24-h hindlimb cast immobilization (HCI) of the predominantly slow-twitch soleus muscle increased intramyocellular diacylglycerol (IMDG) and insulin resistance by activation of lipin1, and HCI
Alessandro Cannavo et al.
Frontiers in pharmacology, 10, 888-888 (2019-08-27)
Hyperaldosteronism alters cardiac function, inducing adverse left ventricle (LV) remodeling either via increased fibrosis deposition, mitochondrial dysfunction, or both. These harmful effects are due, at least in part, to the activation of the G protein-coupled receptor kinase 2 (GRK2). In
我们的科学家团队拥有各种研究领域经验，包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系技术服务部门