Product Name	phospho-IRS1 (Tyr895)
Chinese Name	磷酸化胰岛素受体底物-1抗体
Alias	p-IRS1; IRS1 (phospho T895); IRS1_HUMAN; Insulin receptor substrate 1; IRS-1; IRS 1;
literatures	Specific References  (1)     |     SL3204R has been referenced in 1 publications. [IF=18.962] Xue Li. et al. Dual regulation on oxidative stress and endoplasmic reticulum stress by [70] fullerenes for reversing insulin resistance in diabetes. NANO TODAY. 2022 Aug;45:101541  WB ;  Mouse, Human.   PubMed:10.1016/j.nantod.2022.101541
Product Type	Phosphorylated anti
Research Area	Tumour  Cell biology  immunology  Signal transduction  transcriptional regulatory factor  Diabetes  The cell membrane蛋白
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	(predicted: Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit, )
Applications	WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 （Paraffin sections need antigen repair） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	132kDa
Cellular localization	The cell membrane
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthesised phosphopeptide derived from human IRS1 around the phosphorylation site of Tyr895: GE(p-Y)VN
Lsotype	IgG
Purification	affinity purified by Protein A
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	Insulin receptor substrates (IRS) are responsible for several insulin related activities, such as glucose homeostasis, cell growth, cell transformation, apoptosis and insulin signal transduction. Serine/threonine phosphorylation of IRS1 has been demonstrated to be a negative regulator of insulin signaling and is responsible for its degradation, although IRS1 degradation pathways are not well understood. IRS1 has also been shown to be constitutively activated in cancers such as breast cancer, Wilm's tumors, and adrenal cortical carcinomas, thus making IRS1 phosphorylation and subsequent degradation an attractive therapeutic target. To date there have been four subtypes identified: IRS1, 2, 3 and 4, with IRS1 being widely expressed. 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. Subunit: Interacts with UBTF and PIK3CA. Interacts (via phosphorylated YXXM motifs) with PIK3R1. Interacts with ROCK1 and FER. Interacts (via PH domain) with PHIP. Interacts with GRB2. Interacts with SOCS7. Interacts (via IRS-type PTB domain) with IGF1R and INSR (via the tyrosine-phosphorylated NPXY motif). Interacts with ALK. 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. Phosphorylated by ALK. Phosphorylated at Ser-270, Ser-307, Ser-636 and Ser-1101 by RPS6KB1; phosphorylation induces accelerated degradation of IRS1. DISEASE: Polymorphisms in IRS1 may be involved in the etiology of non-insulin-dependent diabetes mellitus (NIDDM) [MIM:125853]. Similarity: Contains 1 IRS-type PTB domain. Contains 1 PH domain. SWISS: P35568 Gene ID: 3667 Database links: Entrez Gene: 3667 Human Entrez Gene: 16367 Mouse Entrez Gene: 25467 Rat SwissProt: P35568 Human SwissProt: P35569 Mouse SwissProt: P35570 Rat 胰岛素受体底物-1是细胞中分子量为165-185kDa的磷蛋白，胰岛素受体的内源性底物。经胰岛素刺激后其酪氨酸残基被磷酸化。

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