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- W2090116402 endingPage "168" @default.
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- W2090116402 abstract "Signals from the TGF-βs are mediated by the TGF-β receptors and their substrates, the Smad proteins. Inactivation of either of the two transmembrane serine/threonine kinases called the TGF-β type I and type II receptors is now known to underlie a wide variety of human pathologies including, especially carcinogenesis. Numerous studies have now demonstrated that the TGF-β receptor complex and its downstream signaling intermediates constitute a tumor suppressor pathway. We review here a specific pathway of mutational inactivation of the TGF-β type II receptor resulting from microsatellite instability and demonstrate that, by contrast, the most common mechanism of loss of expression of the TGF-β type II receptor involves transcriptional repression. This provides a new target for therapeutic intervention." @default.
- W2090116402 created "2016-06-24" @default.
- W2090116402 creator A5052550785 @default.
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- W2090116402 creator A5078338048 @default.
- W2090116402 creator A5089465499 @default.
- W2090116402 date "2000-04-01" @default.
- W2090116402 modified "2023-10-10" @default.
- W2090116402 title "Molecular mechanisms of inactivation of TGF-β receptors during carcinogenesis" @default.
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- W2090116402 doi "https://doi.org/10.1016/s1359-6101(99)00039-8" @default.
- W2090116402 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10708963" @default.
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