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Mouse Insr Antibody (Center)

Affinity Purified Rabbit Polyclonal Antibody (Pab)

     
  • WB - Mouse Insr Antibody (Center) AP14623c
    Mouse Insr Antibody (Center) (Cat. #AP14623c) western blot analysis in mouse liver tissue lysates (35ug/lane).This demonstrates the Insr antibody detected the Insr protein (arrow).
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Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immuno electron microscopy
  • EIA=Enzyme Immunoassay
WB, E
Primary Accession P15208
Other Accession P15127, NP_034698.2
Reactivity Mouse
Predicted Rat
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 155610 Da
Antigen Region 546-574 aa
Additional Information
Gene ID 16337
Other Names Insulin receptor, IR, CD220, Insulin receptor subunit alpha, Insulin receptor subunit beta, Insr
Target/Specificity This Mouse Insr antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 546-574 amino acids from the Central region of mouse Insr.
Dilution WB~~1:1000
Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsMouse Insr Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name Insr
Function Receptor tyrosine kinase which mediates the pleiotropic actions of insulin (PubMed:38061240). 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). When present in a hybrid receptor with IGF1R, binds IGF1 (By similarity). In adipocytes, inhibits lipolysis (PubMed:27322061).
Cellular Location Cell membrane; Single-pass type I membrane protein. Recycling endosome membrane. Late endosome. Lysosome Note=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
Research Areas
Citations (0)
citation

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Background

This receptor binds insulin and has a tyrosine-protein kinase activity. When present in a hybrid receptor with IGF1R, binds IGF1.

References

Brothers, K.J., et al. Cell Metab. 12(3):295-305(2010)
Divall, S.A., et al. J. Clin. Invest. 120(8):2900-2909(2010)
Fulzele, K., et al. Cell 142(2):309-319(2010)
Ferron, M., et al. Cell 142(2):296-308(2010)
Ulanet, D.B., et al. Proc. Natl. Acad. Sci. U.S.A. 107(24):10791-10798(2010)

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$ 365.00
$ 140.00
Cat# AP14623c
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