Evidence map›Paper›PMID 29858375›Full record

ReviewMolecular cancer research : MCR2018

Understanding the Histone DNA Repair Code: H4K20me2 Makes Its Mark.

Karissa L Paquin, Niall G Howlett

Abstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed.

  1. Review
  2. Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026
    Review
  3. Review
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  13. Review
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  18. Review
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  20. Autism risk gene KMT5B deficiency in prefrontal cortex induces synaptic dysfunction and social deficits via alterations of DNA repair and gene transcription.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Karissa L PaquinDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island.
Niall G HowlettDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island. nhowlett@uri.edu.

Funding

Training CoreP20GM103430 · NIGMS · UNIVERSITY OF RHODE ISLAND · PI Bongsup P Cho · 2012 to 2026
$63.6M
UNDERGRADUATE RESEARCH AND SEMINARSP20RR016457 · NCRR · UNIVERSITY OF RHODE ISLAND · PI SHAKARIAN, ALISON M · 2001 to 2011
$35.5M
Regulation of the Mono-Ubiquitination of the Fanconi Anemia D2 ProteinR01HL101977 · NHLBI · UNIVERSITY OF RHODE ISLAND · PI HOWLETT, NIALL GEORGE · 2011 to 2015
$1.3M
Chromatin State Alterations in Fanconi Anemia Hematologic Disease and Bone Marrow FailureR01HL149907 · NHLBI · UNIVERSITY OF RHODE ISLAND · PI HOWLETT, NIALL GEORGE · 2020 to 2023
$1.2M
NCRR NIH HHS P20 RR016457NHLBI NIH HHS R01 HL101977NHLBI NIH HHS R01 HL149907NIGMS NIH HHS P20 GM103430
6 · The paper itself

Abstract

Chromatin is a highly compact structure that must be rapidly rearranged in order for DNA repair proteins to access sites of damage and facilitate timely and efficient repair. Chromatin plasticity is achieved through multiple processes, including the posttranslational modification of histone tails. In recent years, the impact of histone posttranslational modification on the DNA damage response has become increasingly well recognized, and chromatin plasticity has been firmly linked to efficient DNA repair. One particularly important histone posttranslational modification process is methylation. Here, we focus on the regulation and function of H4K20 methylation (H4K20me) in the DNA damage response and describe the writers, erasers, and readers of this important chromatin mark as well as the combinatorial histone posttranslational modifications that modulate H4K20me recognition. Finally, we discuss the central role of H4K20me in determining if DNA double-strand breaks (DSB) are repaired by the error-prone, nonhomologous DNA end joining pathway or the error-free, homologous recombination pathway. This review article discusses the regulation and function of H4K20me2 in DNA DSB repair and outlines the components and modifications that modulate this important chromatin mark and its fundamental impact on DSB repair pathway choice.

Indexed as

DNA RepairChromatinHistonesHumansPhosphorylationChromatinHistones

Identifiers

PMID29858375
PMCPMC7083049

What OpenQuestion holds

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Registered trials

None linked

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.