04-300 | Anti-phospho-Insulin Receptor (Tyr 1322) Antibody, clone 21G12

100 µg  
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      Key Spec Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      Ca, H, MELISA, WBMPurifiedMonoclonal Antibody
      Catalogue Number04-300
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-phospho-Insulin Receptor (Tyr 1322) Antibody, clone 21G12
      Alternate Names
      • INSR
      Product Information
      • Includes pervanadate treated HEK293 lysate as a positive control.
      PresentationLyophilized in 2X PBS containing 0.09% sodium azide, PEG, and sucrose.
      ApplicationAnti-phospho-Insulin Receptor Antibody, clone 21G12 is an antibody against phospho-Insulin Receptor (Tyr 1322) for use in ELISA & WB.
      Key Applications
      • ELISA
      • Western Blotting
      Biological Information
      ImmunogenKLH-conjugated synthetic peptide encompassing the surrounding amino acids of Tyrosine 1322 on phosphorylated insulin receptor
      SpecificityRecognizes phosphorylated domain of Insulin receptor on Tyrosine 1322.
      Species Reactivity
      • Canine
      • Human
      • Mouse
      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
      • Phosphorylation
      Purification MethodSubsequent thiophilic adsorption 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
      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. Reconstitute prior to use. Reconstitute with 1 mL H2O for 15 min at room temperature. Reconstituted aliquots should be stored frozen at -80°C. Thawed aliquots may be stored at 4°C for up to 3 months. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
      Packaging Information
      Material Size100 µg
      Transport Information
      Supplemental Information




      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 (Mouse monoclonal IgG1) - 2439367 2439367
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 (Mouse monoclonal IgG1) - 1963586 1963586
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 - 2042726 2042726
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 - 2051312 2051312
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 - 2289069 2289069
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 - 2526852 2526852
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 - DAM1528114 DAM1528114
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 - NG1840491 NG1840491
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 - NG1857564 NG1857564
      Anti-phospho-Insulin Receptor (Tyr 1322), clone 21G12 -2615710 2615710


      Reference overviewPub Med ID
      Template to improve glycemic control without reducing adiposity or dietary fat.
      Krishnapuram, R; Dhurandhar, EJ; Dubuisson, O; Kirk-Ballard, H; Bajpeyi, S; Butte, N; Sothern, MS; Larsen-Meyer, E; Chalew, S; Bennett, B; Gupta, AK; Greenway, FL; Johnson, W; Brashear, M; Reinhart, G; Rankinen, T; Bouchard, C; Cefalu, WT; Ye, J; Javier, R; Zuberi, A; Dhurandhar, NV
      American journal of physiology. Endocrinology and metabolism  300  E779-89  2011

      Show Abstract
      21266671 21266671
      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
      Hyperglycemia-induced activation of human T-lymphocytes with de novo emergence of insulin receptors and generation of reactive oxygen species
      Stentz, Frankie B and Kitabchi, Abbas E
      Biochem Biophys Res Commun, 335:491-5 (2005)  2005

      16084832 16084832
      Tyrosine phosphorylation of phosphoinositide-dependent kinase 1 by the insulin receptor is necessary for insulin metabolic signaling
      Fiory, Francesca, et al
      Mol Cell Biol, 25:10803-14 (2005)  2005

      16314505 16314505
      Molecular cloning of a DNA sequence complementary to creatine kinase M mRNA from chickens.
      Schweinfest, CW; Kwiatkowski, RW; Dottin, RP
      Proceedings of the National Academy of Sciences of the United States of America  79  4997-5000  1982

      Show Abstract
      6956910 6956910

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