Evidence map›Paper›PMID 27631103›Full record

ReviewPLoS genetics2016

Acetylation Reader Proteins: Linking Acetylation Signaling to Genome Maintenance and Cancer.

Fade Gong, Li-Ya Chiu, Kyle M Miller

Open access · goldAbstract readReview
In one paragraph

Review in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
7.1field-weighted citation impact, top 2% of its field
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

77 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. LINC00467: an oncogenic long noncoding RNA.Cancer cell international · 2022
    Review
  20. Review

17 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Fade GongDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas, United States of America.
Li-Ya ChiuDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas, United States of America.
Kyle M MillerDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas, United States of America.
The University of Texas at Austin · US

Funding

Shaping DNA Damage Response Networks Via Histone H2A VariantsR01CA198279 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI Kyle M Miller · 2016 to 2026
$3.3M
MECHANISMS OF GENOME MAINTENANCE BY BROMODOMAIN CHROMATIN READER PROTEINSR01CA201268 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI MILLER, KYLE M · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA198279NCI NIH HHS R01 CA201268
6 · The paper itself

Abstract

Chromatin-based DNA damage response (DDR) pathways are fundamental for preventing genome and epigenome instability, which are prevalent in cancer. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) catalyze the addition and removal of acetyl groups on lysine residues, a post-translational modification important for the DDR. Acetylation can alter chromatin structure as well as function by providing binding signals for reader proteins containing acetyl-lysine recognition domains, including the bromodomain (BRD). Acetylation dynamics occur upon DNA damage in part to regulate chromatin and BRD protein interactions that mediate key DDR activities. In cancer, DDR and acetylation pathways are often mutated or abnormally expressed. DNA damaging agents and drugs targeting epigenetic regulators, including HATs, HDACs, and BRD proteins, are used or are being developed to treat cancer. Here, we discuss how histone acetylation pathways, with a focus on acetylation reader proteins, promote genome stability and the DDR. We analyze how acetylation signaling impacts the DDR in the context of cancer and its treatments. Understanding the relationship between epigenetic regulators, the DDR, and chromatin is integral for obtaining a mechanistic understanding of genome and epigenome maintenance pathways, information that can be leveraged for targeting acetylation signaling, and/or the DDR to treat diseases, including cancer.

Indexed as

Epigenesis, GeneticAcetylationChromatinDNA DamageGenome, HumanGenomic InstabilityHistone AcetyltransferasesHistone DeacetylasesHumansNeoplasmsChromatinHistone AcetyltransferasesHistone Deacetylases

Identifiers

PMID27631103
PMCPMC5025232
OpenAlexW2520470932

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.