ARG62523

anti-Insulin Receptor alpha antibody [83-14]

anti-Insulin Receptor alpha antibody [83-14] for ICC/IF,Immunoprecipitation,Inhibition assay,ELISA and Sheep,Cow,Human,Pig

Cancer antibody; Neuroscience antibody; Signaling Transduction antibody

Overview

Product Description Mouse Monoclonal antibody [83-14] recognizes Insulin Receptor alpha
Tested Reactivity Hu, Cow, Pig, Sheep
Species Does Not React With Ms, Rat, Rb
Tested Application ELISA, ICC/IF, IP, Inhib
Host Mouse
Clonality Monoclonal
Clone 83-14
Isotype IgG2a
Target Name Insulin Receptor alpha
Antigen Species Human
Immunogen IM-9 lymphocytes followed by purified insulin receptor.
Epitope aa 469-592 (exon 7/8)
Conjugation Un-conjugated
Alternate Names Insulin receptor; IR; CD220; HHF5; CD antigen CD220; EC 2.7.10.1

Application Instructions

Application Suggestion
Tested Application Dilution
ELISAAssay-dependent
ICC/IFAssay-dependent
IPAssay-dependent
InhibAssay-dependent
Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist.
Positive Control IM-9 lymphocyte cells. Placenta

Properties

Form Liquid
Purification Purified Antibody
Buffer 1X PBS and 0.1% Sodium azide
Preservative 0.1% Sodium azide
Concentration 0.2 mg/ml
Storage Instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C or below. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use.
Note For laboratory research only, not for drug, diagnostic or other use.

Bioinformation

Database Links

GeneID: 3643 Human INSR

Swiss-port # P06213 Human Insulin receptor

Gene Symbol INSR
Gene Full Name insulin receptor
Background 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. [provided by RefSeq, Jul 2008]
Function Receptor tyrosine kinase which mediates the pleiotropic actions of insulin. Binding of insulin leads to phosphorylation of several intracellular substrates, including, insulin receptor substrates (IRS1, 2, 3, 4), SHC, GAB1, CBL and other signaling intermediates. Each of these phosphorylated proteins serve as docking proteins for other signaling proteins that contain Src-homology-2 domains (SH2 domain) that specifically recognize different phosphotyrosines residues, including the p85 regulatory subunit of PI3K and SHP2. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway, which is responsible for most of the metabolic actions of insulin, and the Ras-MAPK pathway, which regulates expression of some genes and cooperates with the PI3K pathway to control cell growth and differentiation. Binding of the SH2 domains of PI3K to phosphotyrosines on IRS1 leads to the activation of PI3K and the generation of phosphatidylinositol-(3, 4, 5)-triphosphate (PIP3), a lipid second messenger, which activates several PIP3-dependent serine/threonine kinases, such as PDPK1 and subsequently AKT/PKB. The net effect of this pathway is to produce a translocation of the glucose transporter SLC2A4/GLUT4 from cytoplasmic vesicles to the cell membrane to facilitate glucose transport. Moreover, upon insulin stimulation, activated AKT/PKB is responsible for: anti-apoptotic effect of insulin by inducing phosphorylation of BAD; regulates the expression of gluconeogenic and lipogenic enzymes by controlling the activity of the winged helix or forkhead (FOX) class of transcription factors. Another pathway regulated by PI3K-AKT/PKB activation is mTORC1 signaling pathway which regulates cell growth and metabolism and integrates signals from insulin. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway. The Ras/RAF/MAP2K/MAPK pathway is mainly involved in mediating cell growth, survival and cellular differentiation of insulin. Phosphorylated IRS1 recruits GRB2/SOS complex, which triggers the activation of the Ras/RAF/MAP2K/MAPK pathway. In addition to binding insulin, the insulin receptor can bind insulin-like growth factors (IGFI and IGFII). Isoform Short has a higher affinity for IGFII binding. When present in a hybrid receptor with IGF1R, binds IGF1. PubMed:12138094 shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin. In contrast, PubMed:16831875 shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin. [UniProt]
Research Area Cancer antibody; Neuroscience antibody; Signaling Transduction antibody
Calculated MW 156 kDa
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 binding to IRS1, SHC1 and STAT5B. Dephosphorylated by PTPRE at Tyr-999, Tyr-1185, Tyr-1189 and Tyr-1190. Dephosphorylated by PTPRF and PTPN1. Dephosphorylated by PTPN2; down-regulates insulin-induced signaling.

Clone References

Two novel mutations in the insulin binding subunit of the insulin receptor gene without insulin binding impairment in a patient with Rabson-Mendenhall syndrome.

ICC/IF / Human

Thiel CT et al.
Mol Genet Metab.,  (2008)

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Glucosamine induces resistance to insulin-like growth factor I (IGF-I) and insulin in Hep G2 cell cultures: biological significance of IGF-I/insulin hybrid receptors.

BL / Human

Sakai K et al.
Endocrinology.,  (2003)

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Increases in free, unbound insulin-like growth factor I enhance insulin responsiveness in human hepatoma G2 cells in culture.

IP / Human

Sakai K et al.
J Biol Chem.,  (2002)

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A region of the insulin receptor important for ligand binding (residues 450-601) is recognized by patients' autoimmune antibodies and inhibitory monoclonal antibodies.

Zhang B et al.
Proc Natl Acad Sci U S A.,  (1991)

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