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Mouse Anti-INSR Recombinant Antibody (11B6) (CBMAB-C2482-LY)

This product is antibody recognizes INSR. The antibody 11B6 immunoassay techniques such as: ELISA, WB.
See all INSR antibodies

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
11B6
Antibody Isotype
IgG1
Application
ELISA, WB

Basic Information

Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

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

Target

Full Name
Insulin Receptor
Introduction
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]
Entrez Gene ID
Human3643
Mouse16337
Rat24954
UniProt ID
HumanP06213
MouseP15208
RatP15127
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 phosphotyrosine 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. In adipocytes, inhibits lipolysis (By similarity).
Biological Process
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
Cellular Location
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.
Involvement in disease
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.
Topology
Extracellular: 763-956
Helical: 957-979
Cytoplasmic: 980-1382
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.

Iraburu, M. J., Garner, T., & Montiel-Duarte, C. (2021). Revising endosomal trafficking under insulin receptor activation. International Journal of Molecular Sciences, 22(13), 6978.

Arcidiacono, B., Chiefari, E., Foryst-Ludwig, A., Curro, G., Navarra, G., Brunetti, F. S., ... & Brunetti, A. (2020). Obesity-related hypoxia via miR-128 decreases insulin-receptor expression in human and mouse adipose tissue promoting systemic insulin resistance. EBioMedicine, 59.

Zhou, B., Liu, J., Zeng, L., Zhu, S., Wang, H., Billiar, T. R., ... & Kang, R. (2020). Extracellular SQSTM1 mediates bacterial septic death in mice through insulin receptor signalling. Nature microbiology, 5(12), 1576-1587.

Fernández-de Frutos, M., Galán-Chilet, I., Goedeke, L., Kim, B., Pardo-Marqués, V., Pérez-García, A., ... & Ramírez, C. M. (2019). MicroRNA 7 Impairs Insulin Signaling and Regulates A β Levels through Posttranscriptional Regulation of the Insulin Receptor Substrate 2, Insulin Receptor, Insulin-Degrading Enzyme, and Liver X Receptor Pathway. Molecular and Cellular Biology, 39(22), e00170-19.

Cignarelli, A., Genchi, V. A., Perrini, S., Natalicchio, A., Laviola, L., & Giorgino, F. (2019). Insulin and insulin receptors in adipose tissue development. International journal of molecular sciences, 20(3), 759.

Payankaulam, S., Raicu, A. M., & Arnosti, D. N. (2019). Transcriptional regulation of INSR, the insulin receptor gene. Genes, 10(12), 984.

Chen, Y., Huang, L., Qi, X., & Chen, C. (2019). Insulin receptor trafficking: consequences for insulin sensitivity and diabetes. International journal of molecular sciences, 20(20), 5007.

Tsai, S., Clemente-Casares, X., Zhou, A. C., Lei, H., Ahn, J. J., Chan, Y. T., ... & Winer, D. A. (2018). Insulin receptor-mediated stimulation boosts T cell immunity during inflammation and infection. Cell metabolism, 28(6), 922-934.

Hersom, M., Helms, H. C., Schmalz, C., Pedersen, T. Å., Buckley, S. T., & Brodin, B. (2018). The insulin receptor is expressed and functional in cultured blood-brain barrier endothelial cells but does not mediate insulin entry from blood to brain. American Journal of Physiology-Endocrinology and Metabolism, 315(4), E531-E542.

Yang, B. Y., Zhai, G., Gong, Y. L., Su, J. Z., Peng, X. Y., Shang, G. H., ... & Xie, S. Q. (2018). Different physiological roles of insulin receptors in mediating nutrient metabolism in zebrafish. American Journal of Physiology-Endocrinology and Metabolism, 315(1), E38-E51.

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For research use only. Not intended for any clinical use.

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