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Molecular mechanisms of inactivation of TGF-β receptors during carcinogenesis

Cited 150 time in Web of Science Cited 159 time in Scopus
Authors
Kim, SJ; Im, YH; Markowitz, SD; Bang, Yung-Jue
Issue Date
2000-03
Citation
Cytokine and Growth Factor Reviews, Vol.11 No.1-2, pp.159-168
Keywords
TGF-betareceptorstumor suppressortranscriptional regulationDNA methylation
Abstract
Signals from the TGF-beta s are mediated by the TGF-beta receptors and their substrates, the Smad proteins. Inactivation of either of the two transmembrane serine/threonine kinases called the TGF-beta 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-beta receptor complex and its downstream signaling intermediates constitute a tumor suppressor pathway. We review here a specific pathway of mutational inactivation of the TGF-beta type II receptor resulting from microsatellite instability and demonstrate that, by contrast. the most common mechanism of loss of expression of the TGF-beta type II receptor involves transcriptional repression. This provides a new target for therapeutic intervention. Published by Elsevier Science Ltd.
ISSN
1359-6101
URI
https://hdl.handle.net/10371/173056
DOI
https://doi.org/10.1016/S1359-6101(99)00039-8
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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