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Background
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Mutations in TSC2 lead to tuberous sclerosis complex. The protein is believed to be a tumor suppressor and is able to specifically stimulate the intrinsic GTPase activity of the Ras-related protein RAP1A and RAB5. The protein associates with hamartin in a cytosolic complex, possibly acting as a chaperone for hamartin. TSC2 may have a function in vesicular transport, but may also play a role in the regulation of cell growth arrest and in the regulation of transcription mediated by steroid receptors. Interaction between TSC1 and TSC2 may facilitate vesicular docking.
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Background
References
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- Li, Y., et al., Mol. Cell. Biol. 24(18):7965-7975 (2004).
- Karbowniczek, M., et al., J. Biol. Chem. 279(29):29930-29937 (2004).
- Corradetti, M.N., et al., Genes Dev. 18(13):1533-1538 (2004).
- Birchenall-Roberts, M.C., et al., J. Biol. Chem. 279(24):25605-25613 (2004).
- Lewis, J.C., et al., J. Med. Genet. 41(3):203-207 (2004).
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