ISR-alpha anticorps (AA 51-150)
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- Antigène Voir toutes ISR-alpha Anticorps
- ISR-alpha (Insulin Receptor alpha (ISR-alpha))
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Épitope
- AA 51-150
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Reactivité
- Humain, Rat
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Hôte
- Lapin
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Clonalité
- Polyclonal
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Conjugué
- Cet anticorp ISR-alpha est non-conjugé
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Application
- Immunofluorescence (Cultured Cells) (IF (cc)), Immunofluorescence (Paraffin-embedded Sections) (IF (p)), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), ELISA, Immunohistochemistry (Frozen Sections) (IHC (fro))
- Réactivité croisée
- Humain, Rat
- Homologie
- Mouse,Dog,Cow,Sheep,Pig,Horse,Rabbit,Guinea Pig
- Purification
- Purified by Protein A.
- Immunogène
- KLH conjugated synthetic peptide derived from human Insulin Receptor Alpha
- Isotype
- IgG
- Top Product
- Discover our top product ISR-alpha Anticorps primaire
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- Indications d'application
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ELISA 1:500-1000
IHC-P 1:200-400
IHC-F 1:100-500
IF(IHC-P) 1:50-200
IF(IHC-F) 1:50-200
IF(ICC) 1:50-200 - Restrictions
- For Research Use only
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- Format
- Liquid
- Concentration
- 1 μg/μL
- Buffer
- 0.01M TBS( pH 7.4) with 1 % BSA, 0.02 % Proclin300 and 50 % Glycerol.
- Agent conservateur
- ProClin
- Précaution d'utilisation
- This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.
- Stock
- 4 °C,-20 °C
- Stockage commentaire
- Shipped at 4°C. Store at -20°C for one year. Avoid repeated freeze/thaw cycles.
- Date de péremption
- 12 months
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- Antigène
- ISR-alpha (Insulin Receptor alpha (ISR-alpha))
- Autre désignation
- Insulin Receptor Alpha (ISR-alpha Produits)
- Synonymes
- anticorps CD220, anticorps HHF5, anticorps insulin receptor, anticorps INSR
- Sujet
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Synonyms: HHF5, CD220, Insulin receptor, IR, INSR
Background: 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.
- ID gène
- 3643
- UniProt
- P06213
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