p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2. Export

@article{citeulike:1270622, abstract = {Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence.}, address = {Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10021, USA. Cell Genesys, Foster City, CA 94405, USA.}, author = {Karlseder, J. and Broccoli, D. and Dai, Y. and Hardy, S. and de Lange, T.}, citeulike-article-id = {1270622}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/10037601}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=10037601}, day = {26}, issn = {0036-8075}, journal = {Science}, keywords = {apoptosis, senescence}, month = {February}, number = {5406}, pages = {1321--1325}, posted-at = {2007-05-01 21:12:11}, priority = {2}, title = {p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/10037601}, volume = {283}, year = {1999} }

TY - JOUR ID - citeulike:1270622 L3 - citeulike-article-id:1270622 N2 - Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence. IS - 5406 JF - Science SN - 0036-8075 AD - Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10021, USA. Cell Genesys, Foster City, CA 94405, USA. EP - 1325 TI - p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2. VL - 283 SP - 1321 KW - apoptosis KW - senescence AU - Karlseder, J AU - Broccoli, D AU - Dai, Y AU - Hardy, S AU - de Lange, T PY - 1999/02/26/ UR - http://view.ncbi.nlm.nih.gov/pubmed/10037601 ER -