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Rabbit Anti-phospho-IRS1 (Ser323)/PE-Cy5 Conjugated antibody (bs-12709R-PE-Cy5)
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說(shuō) 明 書(shū): 100ul  
100ul/2980.00元
大包裝/詢(xún)價(jià)
產(chǎn)品編號(hào) bs-12709R-PE-Cy5
英文名稱(chēng) Rabbit Anti-phospho-IRS1 (Ser323)/PE-Cy5 Conjugated antibody
中文名稱(chēng) PE-Cy5標(biāo)記的磷酸化胰島素受體底物1抗體
別    名 IRS1 (phospho S323); p-IRS1 (phospho S323); HIRS 1; HIRS1; Insulin Receptor Substrate 1; IRS 1; IRS-1; IRS1; IRS1_HUMAN; OTTHUMP00000164234  
規(guī)格價(jià)格 100ul/2980元 購(gòu)買(mǎi)        大包裝/詢(xún)價(jià)
說(shuō) 明 書(shū) 100ul  
產(chǎn)品類(lèi)型 磷酸化抗體 
研究領(lǐng)域 腫瘤  細(xì)胞生物  免疫學(xué)  神經(jīng)生物學(xué)  糖尿病  細(xì)胞膜蛋白  
抗體來(lái)源 Rabbit
克隆類(lèi)型 Polyclonal
交叉反應(yīng) Human, Mouse,  (predicted: Rat, Rabbit, )
產(chǎn)品應(yīng)用 Flow-Cyt=1:50-200 ICC=1:50-200 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 132kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthesised phosphopeptide derived from human IRS1 around the phosphorylation site of Ser323
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
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:
This gene encodes a protein which is phosphorylated by insulin receptor tyrosine kinase. Mutations in this gene are associated with type II diabetes and susceptibility to insulin resistance. [provided by RefSeq, Nov 2009]

Function:
May mediate the control of various cellular processes by insulin. When phosphorylated by the insulin receptor binds specifically to various cellular proteins containing SH2 domains such as phosphatidylinositol 3-kinase p85 subunit or GRB2. Activates phosphatidylinositol 3-kinase when bound to the regulatory p85 subunit.

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

Tissue Specificity:
Isoform Long and isoform Short are predominantly expressed in tissue targets of insulin metabolic effects: liver, adipose tissue and skeletal muscle but are also expressed in the peripheral nerve, kidney, pulmonary alveoli, pancreatic acini, placenta vascular endothelium, fibroblasts, monocytes, granulocytes, erythrocytes and skin. Isoform Short is preferentially expressed in fetal cells such as fetal fibroblasts, muscle, liver and kidney. Found as a hybrid receptor with IGF1R in muscle, heart, kidney, adipose tissue, skeletal muscle, hepatoma, fibroblasts, spleen and placenta (at protein level). Overexpressed in several tumors, including breast, colon, lung, ovary, and thyroid carcinomas.

Post-translational modifications:
Serine phosphorylation of IRS1 is a mechanism for insulin resistance. Ser-312 phosphorylation inhibits insulin action through disruption of IRS1 interaction with the insulin receptor.
Phosphorylation of Tyr-896 is required for GRB2-binding.

DISEASE:
The gene represented in this entry may be involved in disease pathogenesis.
Disease description:A multifactorial disorder of glucose homeostasis caused by a lack of sensitivity to the body's own insulin. Affected individuals usually have an obese body habitus and manifestations of a metabolic syndrome characterized by diabetes, insulin resistance, hypertension and hypertriglyceridemia. The disease results in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.

Similarity:
Contains 1 IRS-type PTB domain.
Contains 1 PH domain.

Database links:

Entrez Gene: 3667 Human

Entrez Gene: 16367 Mouse

Entrez Gene: 25467 Rat

Omim: 147545 Human

SwissProt: P35568 Human

SwissProt: P35569 Mouse

SwissProt: P35570 Rat

Unigene: 471508 Human

Unigene: 4952 Mouse

Unigene: 10476 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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