EGFR Activation by Spatially Restricted Ligands
Abstract
Misregulation of Transforming Growth Factor alpha (TGFalpha) and increased Epidermal Growth Factor Receptor (EGFR) activity has been associated with an increased prognosis of breast cancer (LeMaistre, 1994). TGFalpha and EGFR are required for normal breast development, but deregulation of this signaling pathway can result in uncontrolled proliferation and transformation (Matsui, 1990). 1 am studying the mechanism of TGFalpha activation of EGFR in the model organism Drosophila melanogaster in order to understand how post-transcriptional regulators of TGFalpha function to establish proper ligand expression. The purpose of this project is to identify factors that establish and maintain the tight localization of Gurken (Grk; a Drosophila TGFalpha-like ligand) that is necessary to produce spatially- restricted activation of the EGFR during ovary development (Schupbach, 1987; Neuman- Silberberg & Schupbach, 1993; 1994). These factors could define potential causes of EGFR misregulation, at the level of ligand production, that result in human breast cancer. I am integrating genetic and biochemical methods to study the effects of CG6554, Hrb27C, and Bruno on Grk expression. All three proteins interact with Squid (Sqd), a negative regulator of Grk (Kelly, 1993; Norvell et al. 1999).
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2004
- Accession Number
- ADA426969
Entities
People
- Jennifer S. Goodrich
Organizations
- Princeton University