Weis Center for Research
Biographical Sketch: Gerda E. Breitwieser received her Ph.D. in Molecular Biology from Washington University in St. Louis in 1982. She has been active in the field of GPCR signaling since a postdoctoral fellowship at the University of Texas Medical Branch with Gabor Szabo (1984-1987), which resulted in the seminal demonstration that heterotrimeric G proteins directly regulate ion channels. She continued work on GPCR regulation of ion channels at The Johns Hopkins University School of Medicine, shifting focus to calcium sensing receptors in the mid-1990s. She is currently a Senior Scientist at the Weis Center for Research, Geisinger Clinic. Over the last 15 years, she has dissected the mechanism(s) regulating the function, biosynthesis and trafficking of calcium sensing receptors (CaSR). Recently, the Breitwieser laboratory has made significant contributions to defining the diverse effects of calcimimetics in regulating CaSR function, including characterization of the transmembrane domain binding site for the allosteric drugs NPS 2143 and NPS R-568 (in collaboration with Novartis), and identification of novel intracellular role(s) for calcimimetics, in cotranslational stabilization of newly synthesized CaSR, and in regulation of receptor release to the plasma membrane. The Breitwieser lab has recently defined a unique mechanism regulating CaSR signaling, agonist-driven insertional signaling (ADIS), which accounts for CaSR sensitivity to small changes in agonist concentration and the large dynamic range of signaling output despite the constant presence of agonist.
New Twists on GPCR Trafficking
Trafficking Controls Signaling of the CaSR