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Regulation of smad function by phosphorylation
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research.
2006 (English)In: Smad Signal Transduction: Smads in Proliferation, Diffrentiation and Disease / [ed] Peter ten Dijke, Carl-Henrik Heldin, Dordrecht: Springer, 2006, 235-252 p.Chapter in book (Other (popular science, discussion, etc.))
Abstract [en]

The importance of TGF-β signaling in the suppression of tumorigenesis is supported by the presence of frequent mutations in genes encoding both TGF-β receptors and intermediates in this signaling pathway in cancer. In epithelial cancers sporadic mutations have been found in the genes encoding both the receptor-activated Smad2 (MADH2) and the common intermediate, Smad4 (MADH4). Germline mutations in MADH4 and in BMPR1 (BMP type 1 receptor gene) are the most common mutations in the familial cancer syndrome, Familial Juvenile Polyposis, FJP. More recent studies have revealed epigenetic mechanisms that also play important roles in subverting the function of this pathway. In this chapter, we discuss some of these mechanisms, and provide insight into novel ways in which Smad signaling contributes to the maintenance of tissue homeostasis and ultimately to the suppression of cancer

Place, publisher, year, edition, pages
Dordrecht: Springer, 2006. 235-252 p.
Series
Proteins and Cell Regulation, 5
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-144622DOI: 10.1007/1-4020-4709-6ISBN: 1-4020-4542-5 (print)ISBN: 978-1-4020-4542-4 (print)ISBN: 9781402047091 (print)ISBN: 1402047096 (print)OAI: oai:DiVA.org:uu-144622DiVA: diva2:393841
Available from: 2011-02-01 Created: 2011-02-01 Last updated: 2012-02-08Bibliographically approved

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