|Application ||WB, E|
|Other Accession||NP_000539, 116256352|
|Calculated MW||200608 Da|
|Application Notes||TSC2 antibody can be used for the detection of TSC2 by Western blot at 1 µg/mL.|
|Other Names||TSC2 Antibody: LAM, TSC4, Tuberin, Tuberous sclerosis 2 protein, tuberous sclerosis 2|
|Reconstitution & Storage||TSC2 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||TSC2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||In complex with TSC1, inhibits the nutrient-mediated or growth factor-stimulated phosphorylation of S6K1 and EIF4EBP1 by negatively regulating mTORC1 signaling. Acts as a GTPase- activating protein (GAP) for the small GTPase RHEB, a direct activator of the protein kinase activity of mTORC1. Implicated as a tumor suppressor. Involved in microtubule-mediated protein transport, but this seems to be due to unregulated mTOR signaling. Stimulates weakly the intrinsic GTPase activity of the Ras-related proteins RAP1A and RAB5 in vitro. Mutations in TSC2 lead to constitutive activation of RAP1A in tumors.|
|Cellular Location||Cytoplasm. Membrane; Peripheral membrane protein. Note=At steady state found in association with membranes|
|Tissue Location||Liver, brain, heart, lymphocytes, fibroblasts, biliary epithelium, pancreas, skeletal muscle, kidney, lung and placenta|
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Provided below are standard protocols that you may find useful for product applications.
TSC2 Antibody: Tuberous sclerosis complex (TSC) is an autosomal dominant tumor syndrome caused by mutations in either of the TSC1 or TSC2 tumor suppressor genes. The products of these genes form a protein complex that indirectly decreases the signaling of the mammalian Target of Rapamycin (TOR), an evolutionarily conserved serine/threonine kinase that regulates cell growth and cell cycle through its ability to integrate signals from nutrient levels and growth factors. TOR activity is stimulated by Rheb, a member of the Ras superfamily of G-proteins, when the GTP/GDP ratio bound to Rheb is high. Immunoprecipitated TSC1/TSC2 has been shown to stimulate Rheb GTPase activity in vitro, suggesting that the TSC1/TSC2 complex decreases the ability of Rheb to stimulate TOR activity. This is supported by experiments showing that overexpression of TSC1 and TSC2 results in a significant decrease in the GTP/GDP ratio bound to Rheb and the inhibition of cell growth. At least three isoforms of TSC2 exist.
Shamji AF, Ngheim P, and Schreiber SL. Integration of growth factor and nutrient signaling: implications for cancer biology. Mol. Cell 2003; 12:271-80.
Inoki K, Ouyang H, Li Y, et al. Signaling by target of rapamycin proteins in cell growth control. Microbiol. Mol. Biol. Rev. 2005; 69:79-100.
Tabancay Jr AP, Gau CL, Machado IM, et al. Identification of dominant negative mutants of Rheb GTPase and their use to implicate the involvement of human Rheb in the activation of p70S6K. J. Biol. Chem. 2003; 278:39921-30.
Inoki K, Li Y, Xu T, et al. Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling. Genes Dev. 2003; 17:1829-34.
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