ArticleOncogene2005
Methyltransferase inhibition induces p53-dependent apoptosis and a novel form of cell death.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Oxidative Stress Aggravates Apoptosis of Nucleus Pulposus Cells through mOxidative medicine and cellular longevity · 2022Article
- Inhibition of S-adenosyl-L-homocysteine hydrolase alleviates alloimmune response by down-regulating CD4Annals of translational medicine · 2020Article
- A novel EZH2 inhibitor induces synthetic lethality and apoptosis in PBRM1-deficient cancer cells.Cell cycle (Georgetown, Tex.) · 2020Article
- Protein arginine methylation: an emerging regulator of the cell cycle.Cell division · 2018Review
- Differential effects of AdOx on gene expression in P19 embryonal carcinoma cells.BMC neuroscience · 2012Article
- Deacetylation and methylation at histone H3 lysine 9 (H3K9) coordinate chromosome condensation during cell cycle progression.Molecules and cells · 2011Article
- 8-Cl-adenosine inhibits proliferation and causes apoptosis in B-lymphocytes via protein kinase A-dependent and independent effects: implications for treatment of Carney complex-associated tumors.The Journal of clinical endocrinology and metabolism · 2009Article
- Inhibition of methyltransferases results in induction of g2/m checkpoint and programmed cell death in human T-lymphotropic virus type 1-transformed cells.Journal of virology · 2008Article
- Loss of caspase-9 reveals its essential role for caspase-2 activation and mitochondrial membrane depolarization.Molecular biology of the cell · 2007Article
- Protein methylation is required to maintain optimal HIV-1 infectivity.Retrovirology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have analysed the importance of proper substrate methylation by S-adenosylmethionine-dependent methyltransferases for cell survival and cell cycle progression. We show that treatment of cells with the methyltransferase inhibitor adenosine dialdehyde (AdOx) causes cell cycle arrest and death in different cell types. The phenotypical outcome and form of cell death was strikingly dependent on the AdOx concentration. Lower AdOx concentrations led to a G2 arrest and predominantly caused apoptosis, as judged by biochemical and morphological criteria. Apoptotic cell death was largely dependent on the presence of the tumour suppressor p53, but did not require the Bcl-2 family member Bax. Interestingly, higher concentrations of AdOx led to a novel and so far undescribed form of cell death, which was characterized by distinct, caspase-independent alterations of the cell shape including a marked protuberation of the nucleus, cytoplasmic extensions, actin aggregation, and incomplete chromatin condensation. Although this latter form of cell death was clearly distinguishable from apoptosis, early apoptotic features such as Bax activation were detected, indicating a commitment but incomplete execution of apoptosis. Altogether, these data show that methylation reactions play a distinct role in cell survival, which might influence the decision between different phenotypic forms of cell death.
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Registered trials
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.