Silicon Investor (SI) -- The First Internet Community

STOCKTALK

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor. We ask that you disable ad blocking while on Silicon Investor in the best interests of our community. If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.

Biotech / Medical : Geron Corp. -- Ignore unavailable to you. Want to Upgrade?

To: BulbaMan who wrote (971)	3/25/1998 6:50:00 PM
From: makin_dough99	Respond to of 3576

Call Mike Skillern at CYGS 713-780-1399 for an introduction to what Geron will need in the future.

To: BulbaMan who wrote (971)	3/26/1998 11:48:00 AM
From: Rob-Chemist	Respond to of 3576

Interesting article on telomerase activity and imortilization of cells. From this article, it appears that cells have mechanisms other than telomerase for maintaining telomere length. Mol Carcinog 1998 Jan;21(1):17-25 A repressor function for telomerase activity in telomerase-negative immortal cells. Katoh M, Katoh M, Kameyama M, Kugoh H, Shimizu M, Oshimura M Department of Molecular and Cell Genetics, School of Life Sciences, Faculty of Medicine, Tottori University, Japan. Human telomerase, a ribonucleoprotein that adds TTAGGG repeats onto telomeres and compensates for their shortening, is repressed in most normal human somatic cells. Human somatic cells are considered to have a limited proliferation capacity because of the telomere shortening. Although immortalization of somatic cells is often associated with telomerase reactivation, there are some immortal cells in which telomerase activity is undetectable. In these cells, telomeres may be maintained by an unknown mechanism other than telomerase reactivation. To examine the genetic regulation of telomerase activity, we constructed hybrids between immortal cells with (HepG2) and without (KMST6) telomerase activity. These two cell lines had relatively short and long telomeres, respectively. The hybrid cells continued to proliferate without detectable telomerase activity even after 100 population doublings. Telomerase-positive subpopulations occasionally appeared after serial passages. Southern blot analysis revealed that the hybrids had long terminal restriction fragments similar to that of KMST6, regardless of telomerase activity, and fluorescence in situ hybridization with a telomeric probe showed high-intensity hybridization signals on telomeres, indicating relatively long telomeric repeats. These results suggest that the telomerase-negative immortal cells contain a gene or genes functioning as a telomerase repressor and maintain telomere length by a dominant mechanism other than telomerase reactivation.