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dc.contributor.authorGreider, Carol W.
dc.contributor.authorStrong, Margaret A.
dc.contributor.authorHao, Ling-Yang
dc.date.accessioned2009-11-05T18:09:50Z
dc.date.available2009-11-05T18:09:50Z
dc.date.issued2004-10-22
dc.identifier.citationFirst Published on August 17, 2004, doi: 10.1074/jbc.M403924200 October 22, 2004 The Journal of Biological Chemistry, 279, 45148-45154.en_US
dc.identifier.urihttp://jhir.library.jhu.edu/handle/1774.2/33537
dc.description.abstractEukaryotic cells undergo arrest and enter apoptosis in response to short telomeres. T cells from late generation mTR(-/-) mice that lack telomerase show increased apoptosis when stimulated to enter the cell cycle. The increased apoptosis was not inhibited by colcemid, indicating that the response did not result from breakage of dicentric chromosomes at mitosis. The damage response protein gamma-H2AX localized to telomeres in metaphases from T cells and fibroblasts from mTR(-/-) cells with short telomeres. These data suggest that the major mechanism for induction of apoptosis in late generation mTR(-/-) cells is independent of chromosome segregation and that loss of telomere function through progressive telomere shortening in the absence of telomerase leads to recognition of telomeres as DNA breaks.en_US
dc.language.isoen_USen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biologyen_US
dc.subjectTelomere/ultrastructureen_US
dc.subjectTelomere/metabolismen_US
dc.subjectPhosphorylationen_US
dc.subjectDNA/chemistryen_US
dc.titlePhosphorylation of H2AX at short telomeres in T cells and fibroblastsen_US
dc.typeArticleen_US


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