Rabbit Polyclonal Antibody to Mouse Insr (P1325)

包装: 1G|100G|500G|1KG|100KG

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别名:Insulin receptor, IR, CD220, Insulin receptor subunit alpha, Insulin receptor subunit beta, Insr
应用:WB
反应种属:Human, Mouse, Rat
规格：50μl/100μl

Description
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). When present in a hybrid receptor with IGF1R, binds IGF1 (By similarity).

Description

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). When present in a hybrid receptor with IGF1R, binds IGF1 (By similarity).

Specification
Aliases	Insulin receptor, IR, CD220, Insulin receptor subunit alpha, Insulin receptor subunit beta, Insr
Entrez GeneID	16337
Swissprot	P15208
WB Predicted band size	155.6kDa
Host/Isotype	Rabbit IgG
Storage	Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.
Species Reactivity	Human, Mouse, Rat
Immunogen	This Mouse Insr antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 1325-1358 amino acids from Mouse Insr.
Formulation	Purified polyclonal antibody supplied in PBS with 0.05% sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.

Application
WB	1/2000

Anti-Insr Antibody (P1325) at 1:2000 dilution + mouse kidney lysate

Lysates/proteins at 20 µg per lane.

Secondary
Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution.

Predicted band size : 156 kDa

Blocking/Dilution buffer: 5% NFDM/TBST.

All lanes : Anti-Insr Antibody (P1325) at 1:2000 dilution
Lane 1: L6 whole cell lysate
Lane 2: mouse heart lysate
Lane 3: mouse liver lysate
Lane 4: NIH/3T3 whole cell lysate

Lysates/proteins at 20 µg per lane.

Secondary
Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution.

Predicted band size : 156 kDa

Blocking/Dilution buffer: 5% NFDM/TBST.

本公司的所有产品仅用于科学研究或者工业应用等非医疗目的，不可用于人类或动物的临床诊断或治疗，非药用，非食用。

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