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04-299 Anti-phospho-Insulin Receptor (Tyr 1150/1151) Antibody, clone 10C3

04-299
100 µg  
Purchase on Sigma-Aldrich

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Offerte speciali

Tabella delle specifiche principali

Species ReactivityKey ApplicationsHostFormatAntibody Type
HEnzyme Assays, WBMPurifiedMonoclonal Antibody
Description
Catalogue Number04-299
Brand Family Upstate
Trade Name
  • Upstate
DescriptionAnti-phospho-Insulin Receptor (Tyr 1150/1151) Antibody, clone 10C3
Alternate Names
  • INSR
References
Product Information
FormatPurified
HS Code3002 15 90
Control
  • Includes pervanadate treated HEK293 lysate as a positive control
PresentationIn 1 mL of PBS containing 0.09% sodium azide, PEG, and sucrose and 50% glycerol.
Quality LevelMQ100
Applications
ApplicationDetect phospho-Insulin Receptor (Tyr 1150/1151) using this Anti-phospho-Insulin Receptor (Tyr 1150/1151) Antibody, clone 10C3 validated for use in EA & WB.
Key Applications
  • Enzyme Assays
  • Western Blotting
Biological Information
ImmunogenKLH-conjugated synthetic peptide encompassing the surrounding amino acids of Tyrosine 1150/1151 on phosphorylated insulin receptor.
Clone10C3
HostMouse
SpecificityRecognizes phosphorylated domain of Insulin receptor on Tyrosine 1150/1151.
IsotypeIgG1
Species Reactivity
  • Human
Antibody TypeMonoclonal Antibody
Entrez Gene Number
Entrez Gene SummaryAfter removal of the precursor signal peptide, the insulin receptor precursor is post-translationally cleaved into two chains (alpha and beta) that are covalently linked. Binding of insulin to the insulin receptor (INSR) stimulates glucose uptake. Two transcript variants encoding different isoforms have been found for this gene.
Gene Symbol
  • INSR
  • CD220
  • IR
  • HHF5
Modifications
  • Phosphorylation
Purification MethodThiophilic adsoption and size exclusion chromatography
UniProt Number
UniProt SummaryFUNCTION: SwissProt: P06213 # This receptor binds insulin and has a tyrosine-protein kinase activity. Isoform Short has a higher affinity for insulin. Mediates the metabolic functions of insulin. Binding to insulin stimulates association of the receptor with downstream mediators including IRS1 and phosphatidylinositol 3'-kinase (PI3K). Can activate PI3K either directly by binding to the p85 regulatory subunit, or indirectly via IRS1.
SIZE: 1382 amino acids; 156307 Da
SUBUNIT: Tetramer of 2 alpha and 2 beta chains linked by disulfide bonds. The alpha chains contribute to the formation of the ligand- binding domain, while the beta chains carry the kinase domain. Interacts with SORBS1 but dissociates from it following insulin stimulation. Binds SH2B2. Interacts with the PTB/PID domains of IRS1 and SHC1 in vitro when autophosphorylated on tyrosine residues. The sequences surrounding the phosphorylated NPXY motif contribute differentially to either IRS1 or SHC1 recognition. Interacts with the SH2 domains of the 85 kDa regulatory subunit of PI3K (PIK3R1) in vitro, when autophosphorylated on tyrosine residues. Interacts with SOCS7.
SUBCELLULAR LOCATION: Membrane; Single-pass type I membrane protein.
TISSUE SPECIFICITY: Isoform Long and isoform Short are expressed in the peripheral nerve, kidney, liver, striated muscle, fibroblasts and skin. Isoform Short is expressed also in the spleen and lymphoblasts.
PTM: After being transported from the endoplasmic reticulum to the Golgi apparatus, the single glycosylated precursor is further glycosylated and then cleaved, followed by its transport to the plasma membrane. & Autophosphorylated on tyrosine residues in response to insulin. & Phosphorylation of Tyr-999 is required for IRS1- and SHC1- binding.
DISEASE: SwissProt: P06213 # Defects in INSR are the cause of insulin resistance (Ins resistance) [MIM:125853]. & Defects in INSR are the cause of Rabson-Mendenhall syndrome [MIM:262190]; also known as Mendenhall syndrome. It is a severe insulin resistance syndrome characterized by insulin- resistant diabetes mellitus with pineal hyperplasia and somatic abnormalities. Typical features include coarse, senile-appearing facies, dental and skin abnormalities, abdominal distension, and phallic enlargement. Inheritance is autosomal recessive. & Defects in INSR are the cause of leprechaunism [MIM:246200]; also known as Donohue syndrome. Leprechaunism represents the most severe form of insulin resistance syndrome, characterized by intrauterine and postnatal growth retardation and death in early infancy. Inheritance is autosomal recessive. & Defects in INSR may be associated with noninsulin- dependent diabetes mellitus (NIDDM) [MIM:125853]; also known as diabetes mellitus type 2. & Defects in INSR are the cause of familial hyperinsulinemic hypoglycemia 5 (HHF5) [MIM:609968]. Familial hyperinsulinemic hypoglycemia [MIM:256450], also referred to as congenital hyperinsulinism, nesidioblastosis, or persistent hyperinsulinemic hypoglycemia of infancy (PPHI), is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. & Defects in INSR are the cause of insulin-resistant diabetes mellitus with acanthosis nigricans type A (IRAN type A) [MIM:610549]. This syndrome is characterized by the association of severe insulin resistance (manifested by marked hyperinsulinemia and a failure to respond to exogenous insulin) with the skin lesion acanthosis nigricans and ovarian hyperandrogenism in adolescent female subjects. Women frequently present with hirsutism, acne, amenorrhea or oligomenorrhea, and virilization. This syndrome is different from the type B that has been demonstrated to be secondary to the presence of circulating autoantibodies against the insulin receptor.
SIMILARITY: SwissProt: P06213 ## Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily. & Contains 2 fibronectin type-III domains. & Contains 1 protein kinase domain.
Molecular Weight97 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality AssuranceRoutinely evaluated by immunoblot.
Usage Statement
  • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Storage and Shipping Information
Storage Conditions2 years at -20°C from date of shipment. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
Packaging Information
Material Size100 µg
Transport Information
Supplemental Information
Specifications
Global Trade Item Number
Numero di catalogo GTIN
04-299 04053252581779

Documentation

Anti-phospho-Insulin Receptor (Tyr 1150/1151) Antibody, clone 10C3 Certificati d'Analisi

TitoloNumero di lotto
Anti-phospho-Insulin Receptor (Tyr 1150/1151) 2463614
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 (Mouse monoclonal IgG1) - 2370091 2370091
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 (Mouse monoclonal IgG1) - 2370567 2370567
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 (Mouse monoclonal IgG1) 3113911
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 (Mouse monoclonal IgG1) 2990688
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 (Mouse monoclonal IgG1) - 4043466 4043466
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 (Mouse monoclonal IgG1) - NG1945565 NG1945565
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 - 2139976 2139976
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 - 2495876 2495876
Anti-phospho-Insulin Receptor (Tyr 1150/1151), clone 10C3 - 3245173 3245173

Riferimenti bibliografici

Panoramica dei riferimenti bibliograficiCodice d'identificazione nel Pub Med
Alpha 1,3-fucosyltransferase-VII regulates the signaling molecules of the insulin receptor pathway
Wang, Qiu-yan, et al
FEBS J, 274:526-38 (2007)  2007

17229154 17229154
Hybrid receptors formed by insulin receptor (IR) and insulin-like growth factor I receptor (IGF-IR) have low insulin and high IGF-1 affinity irrespective of the IR splice variant
Slaaby, Rita, et al
J Biol Chem, 281:25869-74 (2006)  2005

16831875 16831875
Effects of hyperglycemia on the differential expression of insulin and insulin-like growth factor-I receptors in human normal peritoneal and adhesion fibroblasts
Rizk, Natalie N, et al
Fertil Steril, 86 Suppl 4:1217-22 (2006)  2005

16962112 16962112

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Categorie

Life Science Research > Antibodies and Assays > Primary Antibodies