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1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF- signaling
1 Department of Molecular Medicine and Gene Therapy, Lund University Hospital, Lund, Sweden; Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University Hospital, Lund, Sweden
2 Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University Hospital, Lund, Sweden; Complex Systems Division, Department of Theoretical Physics, Lund University, Lund, Sweden
3 Department of Cardiology, Heart Lung Center, Utrecht, The Netherlands
4 Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: markus{at}thep.lu.se.
Transforming growth factor beta 1 (TGF-
) regulates cellular functions like proliferation, differentiation and apoptosis. On the cell surface, TGF- binds to receptor complexes consisting of TGF- receptor type II (TRII) and activin like-kinase receptor 5 (Alk5), and the downstream signaling is transduced by Smad- and MAPK proteins. Recent data have shown that alternative receptor combinations besides the classical pairing of TRII/Alk5 can be relevant for TGF- signaling. We have screened for alternative receptors for TGF- and also for gene targets of TGF- signaling, by performing functional assays and microarray analysis in murine embryonic fibroblast (MEF) cell lines lacking Alk5. Data from TGF- stimulated Alk5-/- cells show them to be completely unaffected by TGF-. Additionally, 465 downstream targets of Alk5 signaling were identified when comparing Alk5-/- - or TGF- stimulated Alk5+/+ MEFs with unstimulated Alk5+/+ cells. Our results demonstrate that in MEFs, TGF- signals exclusively through complexes involving Alk5 and give insight to its downstream effector genes.
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