Mouse Anti-INSR Recombinant Antibody (A647) (CBMAB-AP3835LY)

Mouse

Human

A647

IgG

ICC, IHC, IP, WB

Pro622~Thr945

Human

IgG

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Liquid

Affinity purity

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

This gene encodes a member of the receptor tyrosine kinase family of proteins. The encoded preproprotein is proteolytically processed to generate alpha and beta subunits that form a heterotetrameric receptor. Binding of insulin or other ligands to this receptor activates the insulin signaling pathway, which regulates glucose uptake and release, as well as the synthesis and storage of carbohydrates, lipids and protein. Mutations in this gene underlie the inherited severe insulin resistance syndromes including type A insulin resistance syndrome, Donohue syndrome and Rabson-Mendenhall syndrome. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2015]

Insulin Receptor

MAA895Hu23

Activation of protein kinase activityManual Assertion Based On ExperimentIMP:BHF-UCL
Activation of protein kinase B activityManual Assertion Based On ExperimentIDA:BHF-UCL
Adrenal gland developmentIEA:Ensembl
Amyloid-beta clearanceBy SimilarityISS:ARUK-UCL
Carbohydrate metabolic processIEA:UniProtKB-KW
Cellular response to growth factor stimulusIEA:Ensembl
Cellular response to insulin stimulusManual Assertion Based On ExperimentIDA:BHF-UCL
Dendritic spine maintenanceBy SimilarityISS:ARUK-UCL
Epidermis developmentIEA:Ensembl
Exocrine pancreas developmentIEA:Ensembl
G protein-coupled receptor signaling pathwayManual Assertion Based On ExperimentIDA:BHF-UCL
Glucose homeostasisManual Assertion Based On ExperimentIMP:BHF-UCL
Heart morphogenesisManual Assertion Based On ExperimentIMP:BHF-UCL
Insulin receptor signaling pathwayManual Assertion Based On ExperimentIDA:UniProtKB
LearningManual Assertion Based On ExperimentTAS:ARUK-UCL
Male gonad developmentIEA:Ensembl
Male sex determinationIEA:Ensembl
MemoryManual Assertion Based On ExperimentTAS:ARUK-UCL
Neuron projection maintenanceISS:ARUK-UCL
Peptidyl-tyrosine autophosphorylationIEA:Ensembl
Peptidyl-tyrosine phosphorylationManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of cell migrationManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of cell population proliferationManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of developmental growthManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of glucose importManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of glycogen biosynthetic processManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of glycolytic processManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of kinase activityManual Assertion Based On ExperimentIBA:GO_Central
Positive regulation of MAP kinase activityManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of MAPK cascadeManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of meiotic cell cycleIEA:Ensembl
Positive regulation of mitotic nuclear divisionManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of nitric oxide biosynthetic processManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of phosphatidylinositol 3-kinase signalingManual Assertion Based On ExperimentIBA:GO_Central
Positive regulation of protein kinase B signalingManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of protein phosphorylationManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of protein-containing complex disassemblyBy SimilarityISS:ARUK-UCL
Positive regulation of receptor internalizationManual Assertion Based On ExperimentIDA:CACAO
Positive regulation of respiratory burstManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of transcription, DNA-templatedIEA:Ensembl
Protein autophosphorylationManual Assertion Based On ExperimentIDA:BHF-UCL
Protein phosphorylationManual Assertion Based On ExperimentTAS:ARUK-UCL
Receptor-mediated endocytosisBy SimilarityISS:ARUK-UCL
Regulation of embryonic developmentManual Assertion Based On ExperimentIMP:BHF-UCL
Regulation of female gonad developmentIEA:Ensembl
Regulation of transcription, DNA-templatedManual Assertion Based On ExperimentIMP:BHF-UCL
Transmembrane receptor protein tyrosine kinase signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central
Transport across blood-brain barrier2 PublicationsNAS:ARUK-UCL
Viral entry into host cellManual Assertion Based On ExperimentIMP:BHF-UCL

Cell membrane; Late endosome; Lysosome. Binding of insulin to INSR induces internalization and lysosomal degradation of the receptor, a means for down-regulating this signaling pathway after stimulation. In the presence of SORL1, internalized INSR molecules are redirected back to the cell surface, thereby preventing their lysosomal catabolism and strengthening insulin signal reception.

Rabson-Mendenhall syndrome (RMS):
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.
Leprechaunism (LEPRCH):
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.
Diabetes mellitus, non-insulin-dependent (NIDDM):
A multifactorial disorder of glucose homeostasis caused by a lack of sensitivity to the body's own insulin. Affected individuals usually have an obese body habitus and manifestations of a metabolic syndrome characterized by diabetes, insulin resistance, hypertension and hypertriglyceridemia. The disease results in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
Familial hyperinsulinemic hypoglycemia 5 (HHF5):
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.
Insulin-resistant diabetes mellitus with acanthosis nigricans type A (IRAN type A):
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.

Extracellular: 763-956
Helical: 957-979
Cytoplasmic: 980-1382

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.