University of Wisconsin–Madison
College of Agriculture and Life Sciences | School of Medicine and Public Health

Allen Laughon



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 TGFβ signaling.
Research Fields
Development, Gene Expression, Drosophila

Research Description:
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.

Representative Publications:
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.