A part of MilliporeSigma

MAB1138 | Anti-Insulin Receptor αAntibody, α subunit, clone 83-7

100 µg  
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      Key Specifications Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      B, H, Po, Rb, Sh ELISA, FC, IH(P), EA M Purified Monoclonal Antibody
      Catalogue NumberMAB1138
      Brand Family Chemicon®
      Trade Name
      • Chemicon
      DescriptionAnti-Insulin Receptor αAntibody, α subunit, clone 83-7
      Alternate Names
      • CD220
      Product Information
      PresentationLiquid (200μg/mL) in 10mM PBS, pH 7.4, with 0.2% BSA and 15mM sodium azide,
      ApplicationAnti-Insulin Receptor Antibody, α subunit, clone 83-7 is an antibody against Insulin Receptor for use in ELISA, FC, IH(P), EA.
      Key Applications
      • ELISA
      • Flow Cytometry
      • Immunohistochemistry (Paraffin)
      • Enzyme Assay
      Applications Not Recommended
      • Western Blotting
      Application NotesFlow cytometry


      Tyrosine Kinase Assay: antibody mediated capture on microtiter plates

      Does not react with reduced protein in western blots (Soos, 1986).

      Immunohistochemistry (frozen & formalin/paraffin): Use antibody at 2-4μg/mL for 30 minutes at room temperature. (Staining of formalin/paraffin tissues requires digestion of tissue sections with pepsin at 1mg/mL Tris-HCl, pH 2.0 for 15 min. at room temperature or 10 min. at 37°C).

      Optimal working dilutions must be determined by end user.
      Biological Information
      ImmunogenIM-9 lymphocytes followed by purified insulin receptor.
      Epitopealpha subunit
      SpecificityRecognizes the alpha-subunit of insulin receptor (IR). Its epitope is conformational (exon 3) and shows no cross-reaction with IGF-receptors. The analysis was performed using purified receptors and immunoprecipitation followed by western blot using a polyclonal antibody that detects both alpha and beta IR subunits. {Soos. 1986}.

      The human IR is a heterotetrameric membrane glycoprotein consisting of disulfide-linked subunits in a beta-alpha-alpha-beta configuration. The beta-subunit (95kDa) is a single transmembrane domain, whereas the alpha-subunit (135kDa) is completely extracellular.

      SPECIES REACTIVITIES: Reacts with bovine, porcine, rabbit, human, and sheep receptors, does not react with mouse and rat.
      Species Reactivity
      • Bovine
      • Human
      • Pig
      • Rabbit
      • Sheep
      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
      • HHF5
      • IR
      • EC [Contains: Insulin receptor subunit alpha
      • Insulin receptor subunit beta].
      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.
      Physicochemical Information
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      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 ConditionsMaintain at 2-8°C in undiluted aliquots for up to 12 months.
      Packaging Information
      Material Size100 µg
      Transport Information
      Supplemental Information




      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      Anti-Insulin Receptor, subunit, clone 83-7 - 1936864 1936864
      Anti-Insulin Receptor, subunit, clone 83-7 - 2041552 2041552
      Anti-Insulin Receptor, subunit, clone 83-7 - NG1876244 NG1876244
      Anti-Insulin Receptor, subunit, clone 83-7 - NG1915290 NG1915290
      Anti-Insulin Receptor, subunit, clone 83-7 - NG1931175 NG1931175
      Anti-Insulin Receptor, subunit, clone 83-7 - NG1944008 NG1944008
      Anti-Insulin Receptor, α subunit, clone 83-7 - 2398864 2398864
      Anti-Insulin Receptor, α subunit, clone 83-7 -2550577 2550577
      Anti-Insulin Receptor, α subunit, clone 83-7 -2593168 2593168
      Anti-Insulin Receptor, α subunit, clone 83-7 -2610958 2610958
      Anti-Insulin Receptor, α subunit, clone 83-7 -2620644 2620644
      Anti-Insulin Receptor, α subunit, clone 83-7 -2728378 2728378

      Data Sheet

      Anti-Insulin Receptor, alpha subunit, clone 83-7 - Data Sheet

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      Life Science Research > Antibodies and Assays > Primary Antibodies