Position title: Professor
Genetics and Medical Genetics
Smad transcription factors and associated cofactors in response to TGF-beta signaling
- 3432 Genetics/Biotech
- Ph.D., University of Utah (1983) Postdoctoral Research: University of Colorado, Boulder
- Genetics and Medical Genetics
- Research Interests
- We study mechanisms by which Smad transcription factors and associated cofactors regulate transcription in response to TGFÎ² signaling.
- Research Fields
- Development, Gene Expression, Drosophila
We study mechanisms by which TGFbeta signaling pathways control pattern formation. The focus is on Smad proteins, transcription factors that shuttle from cytoplasm to nucleus in response to TGFbeta cytokines. Our past work has shown that Smads bind to target DNAs by means of a conserved amino-terminal domain and that Smad targets in Drosophila are regulated negatively by Brinker. We are currently investigating mechanisms by which Smads repress transcription.
Search PubMed for more publications by Allen Laughon
Cai, Y. and Laughon, A. 2009. The Drosophila Smad cofactor Schnurri engages in redundant and synergistic interactions with multiple corepressors. Biochim Biophys. Acta, 1789, 232-245.
Gao, S. and Laughon, A. 2007. Flexible interation of Drosophila Smad complexes with bipartite binding sites. Biochimica et Biophysica Acta. 1769:484-496.
Gao, S. and Laughon, A. 2006. Decapentaplegic-responsive silencers contain overlapping Mad-binding sites. J. Biol. Chem. 281:25781-25790.
Gao, S., Steffens, J. and Laughon, A. 2005. Dpp-Responsive Silencers are Bound by a Trimeric Mad-Med Complex. J. Biol. Chem. 280: 36158-36164.