ArticleThe Journal of cell biology2009
Induction of alternative lengthening of telomeres-associated PML bodies by p53/p21 requires HP1 proteins.
Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Selective killing of ALT-cancer cells by Withaferin-A involves destabilization of Rad51 and disruption of DNA repair.Cell death & disease · 2026Article
- Orphan nuclear receptors recruit TRIM28 to promote telomeric H3K9me3 for the ALT pathway.The EMBO journal · 2026Article
- Structural organization and function of telomeric chromatin.Nature cell biology · 2026Review
- CHAMP1 complex directs heterochromatin assembly and promotes homology-directed DNA repair.Nature communications · 2025Article
- Porphyromonas gingivalis Outer Membrane Vesicles Promote Apoptosis via msRNA-Regulated DNA Methylation in Periodontitis.Microbiology spectrum · 2023Article
- Recruitment of TRIM33 to cell-context specific PML nuclear bodies regulates nodal signaling in mESCs.The EMBO journal · 2023Article
- A mouse model for Li-Fraumeni-Like Syndrome with cardiac angiosarcomas associated to POT1 mutations.PLoS genetics · 2022Article
- Functional characterization of miR-708 microRNA in telomerase positive and negative human cancer cells.Scientific reports · 2021Article
- Mutations inhibiting KDM4B drive ALT activation in ATRX-mutated glioblastomas.Nature communications · 2021Article
- The Promyelocytic Leukemia Protein facilitates human herpesvirus 6B chromosomal integration, immediate-early 1 protein multiSUMOylation and its localization at telomeres.PLoS pathogens · 2020Article
- Mutant IDH1 Promotes Glioma Formation In Vivo.Cell reports · 2018Article
- Loss of p21 promoted tumorigenesis in the background of telomere dysfunctions induced by TRF2 and Wrn deficiency.International journal of biological sciences · 2018Article
- Withaferin-A kills cancer cells with and without telomerase: chemical, computational and experimental evidences.Cell death & disease · 2017Article
- Essential role of the Cdk2 activator RingoA in meiotic telomere tethering to the nuclear envelope.Nature communications · 2016Article
- Molecular mechanisms of activity and derepression of alternative lengthening of telomeres.Nature structural & molecular biology · 2015Review
- Role of Cdk1 in DNA damage-induced G1 checkpoint abrogation by the human papillomavirus E7 oncogene.Cell cycle (Georgetown, Tex.) · 2014Article
- The telomere-associated homeobox-containing protein TAH1/HMBOX1 participates in telomere maintenance in ALT cells.Journal of cell science · 2013Article
- Modulation of telomeres in alternative lengthening of telomeres type I like human cells by the expression of werner protein and telomerase.Journal of oncology · 2012Article
- HP1-mediated formation of alternative lengthening of telomeres-associated PML bodies requires HIRA but not ASF1a.PloS one · 2011Article
- p53 and p21(Waf1) are recruited to distinct PML-containing nuclear foci in irradiated and Nutlin-3a-treated U2OS cells.Journal of cellular biochemistry · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.