Applications: WB, IHC
Host: Mouse monoclonal
WB, IHC, IHC-P, PEP-ELISAHost:
Applications: WB, ELISA, PA
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 decreases the ability of Rheb to stimulate TOR activity. This is supported by experiments showing overexpression of TSC1 and TSC2 results in a significant decrease in the GTP/GDP ratio bound to Rheb and the inhibition of cell growth. A shorter 40 kDa isoform of TSC1 has been shown to exist but its function is unknown
Bioinformatics Tool for TSC1
Discover related pathways, diseases and genes to TSC1. Need help? Read the Bioinformatics Tool Guide
for instructions on using this tool.
Related TSC1 Blog Posts
Check out the latest blog posts on TSC1.
Read more TSC1 related blogs.
|TSC1 - a negative regulator of mTOR signaling
TSC1 is a tumor suppressor gene that encodes a 130 kDa protein called hamartin. TSC1 was first identified as an oncogenic driver of Tuberous Sclerosis, a condition characterized by numerous benign tumors of the skin, brain, heart, and lungs. A mut... Read more.