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Eur. J. Clin. Invest. · Dec 2009
CDKs as therapeutic targets for the human genetic disease tuberous sclerosis?
- M Rosner, H Dolznig, C Fuchs, N Siegel, A Valli, and M Hengstschläger.
- Medical University of Vienna, Vienna, Austria.
- Eur. J. Clin. Invest. 2009 Dec 1; 39 (12): 1033-5.
AbstractThe tuberous sclerosis gene 2 product tuberin is an important regulator of the mammalian target of rapamycin (mTOR). In addition, tuberin is known to bind to the cyclin-dependent kinase (CDK) inhibitor p27(Kip1) (p27) and to regulate its stability and localization via mTOR-independent mechanisms. Recently, evidence has been provided that tuberin also affects p27 localization via regulating mTOR's potential to activate the serum- and glucocorticoid-inducible kinase (SGK1) to phosphorylate p27. Taken together, these findings strengthen the argument that besides mTOR-inhibitors, such as rapamycin analogues, p27 and CDKs could also be considered targets for hamartoma therapeutics in tuberous sclerosis.
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