ArticleCancer research2011
MDC1 cleavage by caspase-3: a novel mechanism for inactivating the DNA damage response during apoptosis.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Review
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- Molecular Pathogenesis of Radiation-Induced Cell Toxicity in Stem Cells.International journal of molecular sciences · 2017Review
- DNA damage precedes apoptosis during the regression of the interdigital tissue in vertebrate embryos.Scientific reports · 2016Article
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- The nuclear γ-H2AX apoptotic ring: implications for cancers and autoimmune diseases.Cellular and molecular life sciences : CMLS · 2014Review
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- Customized chemotherapy in metastatic non-small cell lung cancer (NSCLC).Translational lung cancer research · 2013Review
- Heat shock protein 90α (HSP90α), a substrate and chaperone of DNA-PK necessary for the apoptotic response.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Analysis of apoptosis methods recently used in Cancer Research and Cell Death & Disease publications.Cell death & disease · 2012Article
- Mitochondrial superoxide anions induced by exogenous oxidative stress determine tumor cell fate: an individual cell-based study.Journal of Zhejiang University. Science. BArticle
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 2 institutions in 1 country.
Funding
Abstract
Recently, we identified the "apoptotic ring," containing phosphorylated histone H2AX (γ-H2AX), as an early chromatin modification during apoptosis. Because γ-H2AX initiates the DNA damage response (DDR), we tested whether the apoptotic H2AX response leads to the full recruitment of the DDR factors that normally coordinate DNA repair and cell-cycle checkpoints. We show that the apoptotic H2AX response does not recruit the DDR factors because MDC1 (mediator of DNA damage checkpoint protein 1), which normally binds to γ-H2AX in response to DNA damage and amplifies the DDR, is cleaved by caspase-3. This cleavage separates the BRCT and FHA domains of MDC1 and constitutes a novel mechanism for the inactivation of DNA repair in apoptotic cells. Also, we show that downregulation of MDC1 increases the apoptotic response to TRAIL. Together, these results implicate MDC1 in the cellular apoptotic response.
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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.