• merck millipore,默克密理博,MAB1138,Anti-Insulin Receptor αAntibody, α subunit, clone 83-7
  • merck millipore,默克密理博,MAB1138,Anti-Insulin Receptor αAntibody, α subunit, clone 83-7

    产品名称:Anti-Insulin Receptor αAntibody, α subunit, clone 83-7
    产品型号:MAB1138
    Anti-Insulin Receptor Antibody, α subunit, clone 83-7 is an antibody against Insulin Receptor for use in ELISA, FC, IH(P), EA.

    merck millipore,默克密理博,MAB1138,Anti-Insulin Receptor αAntibody, α subunit, clone 83-7

  • 产品介绍
  • merck millipore,默克密理博,MAB1138,Anti-Insulin Receptor αAntibody, α subunit, clone 83-7

    重要规格表

    品种反应性 主要应用 宿主 格式 抗体类型
    Sh, B, H, Po, RbFC, ELISAMPurifiedMonoclonal Antibody
    描述
    产品目录编号 MAB1138
    Replaces CBL241
    品牌系列 Chemicon®
    商名
    • Chemicon
    描述 Anti-Insulin Receptor αAntibody, α subunit, clone 83-7
    Alternate Names
    • CD220
    产品信息
    格式 Purified
    演示 Liquid (200μg/mL) in 10mM PBS, pH 7.4, with 0.2% BSA and 15mM sodium azide,
    应用
    应用 Anti-Insulin Receptor Antibody, α subunit, clone 83-7 is an antibody against Insulin Receptor for use in ELISA, FC, IH(P), EA.
    主要应用
    • Flow Cytometry
    • ELISA
    不建议的应用
    • Western Blotting
    应用说明 Flow cytometry

    ELISA

    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.
    生物信息
    免疫原品种 IM-9 lymphocytes followed by purified insulin receptor.
    表位 alpha subunit
    克隆 83-7
    宿主 Mouse
    特异性 Recognizes 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.
    同种型 IgG1
    品种反应性 SheepBovineHumanPigRabbit
    抗体类型 Monoclonal Antibody
    Entrez基因编号
    • NM_001079817.1
    • NM_000208.2
    Entrez基因汇总 After 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.
    基因符号
    • Insulin receptor subunit beta].
    • INSR
    • CD220
    • HHF5
    • IR
    • EC 2.7.10.1 [Contains: Insulin receptor subunit alpha
    UniProt编号
    • P06213
    UniProt汇总 FUNCTION: 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.
    产品使用声明
    使用声明
    • 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.
    储存和货运信息
    存储条件 Maintain at 2-8°C in undiluted aliquots for up to 12 months.
    包装信息
    数量 100 µg

    merck millipore,默克密理博,MAB1138,Anti-Insulin Receptor αAntibody, α subunit, clone 83-7

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