Lack of Replicative Senescence in Normal Rodent Glia
- 2 February 2001
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 291 (5505), 872-875
- https://doi.org/10.1126/science.1056782
Abstract
Replicative senescence is thought to be an intrinsic mechanism for limiting the proliferative life-span of normal somatic cells. We show here that rat Schwann cells can be expanded indefinitely in culture while maintaining checkpoints normally lost during the immortalization process. These findings demonstrate that senescence is not an inevitable consequence of extended proliferation in culture.Keywords
This publication has 16 references indexed in Scilit:
- Cellular SenescenceCell, 2000
- Extension of Life-Span by Introduction of Telomerase into Normal Human CellsScience, 1998
- Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and agingOncogene, 1997
- The biology of replicative senescenceEuropean Journal Of Cancer, 1997
- Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4aCell, 1997
- Cooperating oncogenes converge to regulate cyclin/cdk complexes.Genes & Development, 1997
- Calcitonin gene-related peptide promotes Schwann cell proliferation.The Journal of cell biology, 1995
- Specific Association of Human Telomerase Activity with Immortal Cells and CancerScience, 1994
- DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts.Genes & Development, 1994
- Studies on cultured rat Schwann cells. I. Establishment of purified populations from cultures of peripheral nerveBrain Research, 1979