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.
TSC2 antibody can be used in ELISA, Western Blot starting at 1:2000, immunohistochemistry starting at 1:50, and immunoprecipitation
Phosphate-buffered solution, pH 7.2, 0.09% sodium azide, 50% glycerol.
Aliquot and store at -20°C or below. Avoid multiple freeze-thaw cycles.