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• W2117992438 abstract "Alternative lengthening of telomeres (ALT) is a recombination-mediated process that maintains telomeres in telomerase-negative cancer cells. In asynchronously dividing ALT-positive cell populations, a small fraction of the cells have ALT-associated promyelocytic leukemia nuclear bodies (APBs), which contain (TTAGGG)n DNA and telomere-binding proteins. We found that restoring p53 function in ALT cells caused p21 up-regulation, growth arrest/senescence, and a large increase in cells containing APBs. Knockdown of p21 significantly reduced p53-mediated induction of APBs. Moreover, we found that heterochromatin protein 1 (HP1) is present in APBs, and knockdown of HP1alpha and/or HP1gamma prevented p53-mediated APB induction, which suggests that HP1-mediated chromatin compaction is required for APB formation. Therefore, although the presence of APBs in a cell line or tumor is an excellent qualitative marker for ALT, the association of APBs with growth arrest/senescence and with closed telomeric chromatin, which is likely to repress recombination, suggests there is no simple correlation between ALT activity level and the number of APBs or APB-positive cells." @default.
• W2117992438 created "2016-06-24" @default.
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• W2117992438 creator A5029629862 @default.
• W2117992438 creator A5050482798 @default.
• W2117992438 date "2009-05-25" @default.
• W2117992438 modified "2023-10-13" @default.
• W2117992438 title "Induction of alternative lengthening of telomeres-associated PML bodies by p53/p21 requires HP1 proteins" @default.
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• W2117992438 doi "https://doi.org/10.1083/jcb.200810084" @default.
• W2117992438 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2711592" @default.
• W2117992438 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19468068" @default.
• W2117992438 hasPublicationYear "2009" @default.
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