The MH1 domains of Smad2 and Smad3 are involved in the regulation of the ALK7 signals

Citation
R. Watanabe et al., The MH1 domains of Smad2 and Smad3 are involved in the regulation of the ALK7 signals, BIOC BIOP R, 254(3), 1999, pp. 707-712
Citations number
19
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN journal
0006-291X → ACNP
Volume
254
Issue
3
Year of publication
1999
Pages
707 - 712
Database
ISI
SICI code
0006-291X(19990127)254:3<707:TMDOSA>2.0.ZU;2-1
Abstract
The biological responses of the transforming growth factor beta (TGF-beta) superfamily are induced by activation of a receptor complex and Smad protei ns. We surveyed the TGF-beta superfamily receptors using the degenerate PCR strategy, and found activin receptor-like kinase 7 (ALK7) to be abundantly expressed in fetal rat pancreatic islets. ALK7 is also expressed in adult rat islets and pancreatic beta-cell-derived MING cells. The constitutively active form of ALK7, ALK7(T194D), activated Smad3 and a chimeric Smad prote in, Smad3-2, containing the MH1 domain of Smad3 and the MH2 domain of Smad2 , and translocated them to nuclei and then induced activation of the human PAI-1 promoter. However, neither Smad2 nor Smad2-3 protein, containing the MH1 domain of Smad2 and the MH2 domain of Smad3 were activated. These resul ts indicate that the ALK7 signal regulates nuclear localization and activat ion of Smad2 and Smad3, and the MH1 domain of Smad2 has inhibitory effects on the nuclear localization. (C) 1999 Academic Press.