ALT Telomeres Get Together with Nuclear Receptors
Author(s) -
Eric Aeby,
Joachim Lingner
Publication year - 2015
Publication title -
cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 26.304
H-Index - 776
eISSN - 1097-4172
pISSN - 0092-8674
DOI - 10.1016/j.cell.2015.02.006
Subject(s) - telomere , biology , telomerase , homologous recombination , chromatin , genetics , chromosome , homologous chromosome , receptor , recombination , microbiology and biotechnology , nuclear receptor , dna , gene , transcription factor
Nuclear receptors bind chromosome ends in "alternative lengthening of telomeres" (ALT) cancer cells that maintain their ends by homologous recombination instead of telomerase. Marzec et al. now demonstrate that, in ALT cells, nuclear receptors not only trigger distal chromatin associations to mediate telomere-telomere recombination events, but also drive chromosome-internal targeted telomere insertions (TTI).
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