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FOR IMMEDIATE RELEASE
November 30, 2007
Penn Presentations at American Society of Cell Biology Annual Meeting Touch on Cancer, Neurodegenerative Diseases, and Muscular Dystrophy
WASHINGTON, DC – Among the 72 posters, lectures, and mini-symposia given by University of Pennsylvania researchers at the ASCB annual meeting are talks that present new research findings on the molecular workings of several types of diseases.
The 47th annual meeting of the American Society of Cell Biology takes place on December 1-5, 2007 in Washington, D.C.
Some highlights are:
Huntington's Disease: A new role has been discovered for huntingtin (Htt), the defective protein in Huntington's Disease. Htt is crucial for the movement of packets inside cells that recycle and transport important molecules. Disruption of this movement by mutant Htt may help explain the nerve degeneration seen in Huntington's disease. These findings are presented by J. P. Caviston and E. L. F. Holzbaur of the Department of Physiology. (#2091, Poster 12/4)
Lou Gehrig's Disease (ALS): Nerve degeneration diseases such as ALS may be caused by disruption of molecular signaling, a normal process that involves transport of critical signal molecules from the nerve synapse into the nerve cell body. The study was conducted by E. Perlson, J. Ross, K. Wallace, R. Dixit, G. Jeong, R. Kalb, and E. L. Holzbaur of the Department of Physiology. (#1659, Poster, 12/4)
Muscular Dystrophies (MD): Some MDs are caused by the failure of muscle cells to adhere to a structural scaffold so that they can withstand cell-generated tension. Paxillin, a protein that is more abundant in some muscular dystrophies, may cause the dystrophic cells to be overly tense. This study was conducted by M. Tewari, S. Sen, A. Engler, M. Zad, and D. E. Discher of the School of Arts and Sciences, P. Acousta and H. L. Sweeney of the Pennsylvania Muscle Institute and Department of Physiology, and E. Barton of the Dental School. (#1389, Poster, 12/3)
Cancer: An enzyme required for normal growth and development, called ATE1, may be a tumor suppressor. Cells from mice that had the ATE1 gene knocked out were able to cause tumors when transplanted into normal mice. This finding is presented by R. R. Rai and A. Kashina of the Animal Biology Department. (#1533, Poster, 12/3)
Cancer: A protein called Rap1 is involved in tumor cell migration. It is located in cell motile “feet,” and is over-expressed in surgical specimens of infiltrating cancers of the breast. This study was conducted by W. S. Y. Lee and N. Kushnir of the Department of Microbiology, D. K. Furstenau and M. J. L. Dela Cruz of the Department of Surgery, and M. A. Guvakova of both departments. (#398, Poster, 12/2)
Editor’s Note: Use presentation number and date listed after each entry to locate the Penn talks for your meeting itinerary.
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Release available online at http://www.uphs.upenn.edu/news/News_Releases/nov07/