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TSC2, CT (Tuberous Sclerosis Complex 2, Tuberous Sclerosis 2 Protein, FLJ43106, LAM, TSC4, Tuberin)

Cat no: T9100-25R


Supplier: United States Biological
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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. Applications: Suitable for use in Western Blot. Other applications not tested. Recommended Dilution: Western Blot: 1ug/ml Optimal dilutions to be determined by the researcher. Positive Control: L1210 cell lysate Storage and Stability: May be stored at 4 degrees C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
Catalogue number: T9100-25R
Reactivities: Human, Mouse
Hosts: Rabbit
Applications: Western Blot
Size: 50ug
Form: Supplied as a liquid in PBS, 0.02% sodium azide.
P type: Pab
Isotype: IgG
Purity: Purified by immunoaffinity chromatography.
References: 1. Shamji AF, Ngheim P, and Schreiber SL. Integration of growth factor and nutrient signaling: implications for cancer biology. Mol. Cell 2003;12:271-80. 2. 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. 3. 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. 4. 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. 5. Tee AR, Fingar DC, Manning BD, et al. Tuberous sclerosis complex-1 and -2 gene products function together to inhibit mammalian target of rapamycin (mTOR)-mediated downstream signaling. Proc. Natl. Acad. Sci. USA 2002;99:13571-6.
Additional info: Recognizes human TSC2 (CT). Species Crossreactivity: mouse.

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