Abstract
Recent genetic studies of Drosophila melanogaster and subsequent biochemical analysis in mammalian cells revealed that products of tuberous sclerosis genes, TSC1 and TSC2, regulate insulin signaling via suppression of p70 ribosomal S6 subunit-kinase (S6K) activity. In this study, using transplantation in the nude mouse, we found that the growth of a renal tumor cell line from Tsc2 knockout mouse was suppressed by the treatment of rapamycin, an inhibitor of mTOR (mammalian target of rapamycin) which is an upstream activator of S6K. The robust in vivo effect of rapamycin suggests that it can be used for chemotherapy of tuberous sclerosis-associated hamartomas and tumors. Other yet undiscovered chemicals selectively downregulate mTOR-S6K pathway may provide new therapeutic drugs for tuberous sclerosis.(Communicated by Takashi SUGIMURA, M. J. A., Jan. 14, 2003)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
