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Anti-Insulin Receptor Beta (Tyr1355), ALEXA Fluor 594

Anti-Insulin Receptor Beta (Tyr1355), ALEXA Fluor 594 size: 100 microliters 516

Price 516
Size 100 microliters
TypeConjugated Primary Antibody
Conjugated with 594, ALEXA FLUOR®
Host organismRabbit (Oryctolagus cuniculus)
Target Protein/PeptideInsulin Receptor Beta Tyr1355
SpecificityThis antibody reacts specifically with Insulin Receptor Beta (Tyr1355)
ModificationPhosphorylation
Modification siteTyr1355
ClonalityPolyclonal Antibody
ClonePolyclonal Antibodies
Concentration1ug per 1ul
Subcellular locationsCytoplasm
Antigen SourceKLH conjugated synthetic phosphopeptide derived from human Insulin Receptor beta around the phosphorylation site of Tyr1355 [RS(p-Y)EE]
Gene ID3643
Swiss ProtP06213
ApplicationsIF(IHC-P)
Applications with corresponding dilutionsIF(IHC-P)(1:50-200)
Cross reactive speciesHuman (Homo sapiens)
Cross Reactive Species details However, note that due to limited knowledge it is impossible to predict with 100% guarantee that the antibody does not corss react with any other species, No significant cross reactivity has been observed for this antibody for the tested species
Background information 2, 3, 4, 4), 5)-triphosphate (PIP3), AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway, Another pathway regulated by PI3K-AKT/PKB activation is mTORC1 signaling pathway which regulates cell growth and metabolism and integrates signals from insulin, Binding of insulin leads to phosphorylation of several intracellular substrates, Binding of the SH2 domains of PI3K to phosphotyrosines on IRS1 leads to the activation of PI3K and the generation of phosphatidylinositol-(3, 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, GAB1, Moreover, Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway, SHC, 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, a lipid second messenger, activated AKT/PKB is responsible for: anti-apoptotic effect of insulin by inducing phosphorylation of BAD, and the Ras-MAPK pathway, including, including the p85 regulatory subunit of PI3K and SHP2, insulin receptor substrates (IRS1, regulates the expression of gluconeogenic and lipogenic enzymes by controlling the activity of the winged helix or forkhead (FOX) class of transcription factors, such as PDPK1 and subsequently AKT/PKB, upon insulin stimulation, which activates several PIP3-dependent serine/threonine kinases, which is responsible for most of the metabolic actions of insulin, which regulates expression of some genes and cooperates with the PI3K pathway to control cell growth and differentiation, Receptor tyrosine kinase which mediates the pleiotropic actions of insulin
Purification methodPurified by Protein A
Storage 50% glycerol and 0, Store at 4°, 09% sodium azide, C for 12 months, Water buffered solution containing 100ug/ml BSA
Excitation emission590nm/617nm
Synonyms CD220, INSR, IR, Insulin receptor, HHF5
Also known asInsulin Receptor Beta (Tyr1355) Antibody
Other nameAnti-Insulin Receptor Beta (Tyr1355)
Advisory For antibodies that are in liquid form or reconstituted lyophilized antibodies small amounts could become entrapped on the seal or the walls of the tube, Prior to use briefly centrifuge the vial to gather all the solution on the bottom, specificity and sensitivity, thus reducing its reactivity, Avoid freeze/thaw cycles as they may denaturate the polypeptide chains of the antibody
PropertiesFor facs or microscopy Alexa 1 conjugate
ConjugationAlexa Fluor
Gene targetInsulin Receptor Beta (Tyr1355)
Short nameAnti-Insulin Receptor Beta (Tyr1355) Fluor 594
LabelALEXA
Alternative name ALEXA Fluor 594, antibody to-Insulin Receptor b (Tyr1355)

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