Elaine Alarid

Position title: Professor, Oncology

Email: alarid@oncology.wisc.edu

Phone: Estrogen Response


BA 1985 University of California-Berkeley, Berkeley, California
PhD 1991 University of California-Berkeley, Berkeley, California
Postdoctoral Position: University of California-San Francisco

Elaine Alarid. Professor, Oncology. Estrogen Response.

PubMed Publications

Research Focus

My long-time research interest has been in the regulation of hormone action in development and cancer. I have extensive research training in comparative, human and molecular endocrinology using in vivo and in vitro techniques through the laboratories of Howard Bern, Carl Nicoll, Gerry Cunha, and Pamela Mellon. I was also fortunate to work with Jack Gorski. My laboratories current research focuses on the regulation of hormonal sensitivity through control of receptors. In particular, we have used ERα as a model system to understand how changes in receptor number impact ERα function and tumor cell biology. We are well positioned to complete the proposed aims of the study. We co-discovered proteolysis as a regulatory mechanism governing ERα levels in cancer cells; a finding which later proved to be generally applicable to other steroid hormone receptors. We have a continuous publication record examining the regulation of ERα protein and gene expression by the proteasome and phosphorylation. We also identified the functional consequences of altered levels of ERα protein on ERα transcriptional function, and contributed to studies to establish a quantitative measure of ERα content in human breast cancer cohorts. We identified the importance of N-terminal S118 residue in the regulation of ERα protein levels and using models developed in our laboratory, showed that transcriptional regulation of endogenous ERα target genes through this site can be explained by changes in recruitment of coactivators to the ERα C-terminus. These studies also linked proteolysis to recruitment of ubiquitin ligases to target promoters and post-translational modification of ERα by ubiquitination. The latter contributed not only to an improved understanding of ERα protein and transcriptional regulation, but generated tools (stable cell lines, mutant ERα constructs) that have been distributed to a laboratories world-wide for studies of ERα.

Program Activities

  • Joined ERP Program: 1999
  • Former ERP T32 Steering Committee Member


No past or current ERP students