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Role of Smads in TGFβ signaling
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, Faculty of Medicine, Department of Medical Biochemistry and Microbiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research. Uppsala University, Science for Life Laboratory, SciLifeLab.
2012 (English)In: Cell and Tissue Research, ISSN 0302-766X, E-ISSN 1432-0878, Vol. 347, no 1, 21-36 p.Article, review/survey (Refereed) Published
Abstract [en]

Transforming growth factor-β (TGFβ) is the prototype for a large family of pleiotropic factors that signal via heterotetrameric complexes of type I and type II serine/threonine kinase receptors. Important intracellular mediators of TGFβ signaling are members of the Smad family. Smad2 and 3 are activated by C-terminal receptor-mediated phosphorylation, whereafter they form complexes with Smad4 and are translocated to the nucleus where they, in cooperation with other transcription factors, co-activators and co-repressors, regulate the transcription of specific genes. Smads have key roles in exerting TGFβ-induced programs leading to cell growth arrest and epithelial-mesenchymal transition. The activity and stability of Smad molecules are carefully regulated by a plethora of post-translational modifications, including phosphorylation, ubiquitination, sumoylation, acetylation and poly(ADP)-ribosylation. The Smad function has been shown to be perturbed in certain diseases such as cancer.

Place, publisher, year, edition, pages
2012. Vol. 347, no 1, 21-36 p.
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Medical and Health Sciences
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URN: urn:nbn:se:uu:diva-159991DOI: 10.1007/s00441-011-1190-xISI: 000298800700005PubMedID: 21643690OAI: oai:DiVA.org:uu-159991DiVA: diva2:447730
Available from: 2011-10-13 Created: 2011-10-13 Last updated: 2017-12-08Bibliographically approved

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Heldin, Carl-HenrikMoustakas, Aristidis

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Ludwig Institute for Cancer ResearchDepartment of Medical Biochemistry and MicrobiologyScience for Life Laboratory, SciLifeLab
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