Factors That Effect Signal Transduction by the Estrogen Receptor.
Annual rept. 1 Oct 96-31 Sep 97,
NEW YORK UNIV MEDICAL CENTER NY
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The goal of this proposal is to identify and characterize proteins involved in signaling by the estrogen receptor ER, a transcription factor involved in many human breast tumors, using genetic strategies. Through dosage suppression analysis, we have isolated a gene that when overexpressed dramatically increases ER transcriptional activity. The gene is the yeast homologue of the human p23 protein, a component of the molecular chaperonin complex bound to many unliganded steroid receptors. The cellular distribution of p23 is mostly cytoplasmic, however, this pattern is altered upon expression of ER, whereupon p23 colocalizes with ER in the nucleus. This colocalization was seen in the absence of estrogen addition of estrogen results in redistribution of p23 to the cytoplasm. Our work suggests that p23 is a positive regulator of ER, and therefore a possible means by which to control ER function and stop breast cancer growth.
- Anatomy and Physiology