Evidence map›Paper›PMID 29393731›Full record

ArticleCell cycle (Georgetown, Tex.)2018

Double duty: ZMYND8 in the DNA damage response and cancer.

Fade Gong, Kyle M Miller

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. RACK7 Interacts with PRC2 Complex to Regulate Astrocyte Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Joining the PARty: PARP Regulation of KDM5A during DNA Repair (and Transcription?).BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
    Review
  14. Review
  15. Validation of ZMYND8 as a new treatment target in hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2021
    Article
  16. Article
  17. Regulation of ZMYND8 to Treat Cancer.Molecules (Basel, Switzerland) · 2021
    Review
  18. Article
  19. Review
  20. Review
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 at 1 institution in 1 country.

Fade Gonga Department of Molecular Biosciences, Institute for Cellular and Molecular Biology , The University of Texas at Austin , 2506 Speedway, Austin , TX 78712 , USA.
Kyle M Millera Department of Molecular Biosciences, Institute for Cellular and Molecular Biology , The University of Texas at Austin , 2506 Speedway, Austin , TX 78712 , USA.ORCID 0000-0002-4544-0013
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

Our genetic information is organized into chromatin, which consists of histones and proteins involved in regulating DNA compaction, accessibility and function. Chromatin is decorated by histone modifications, which provide signals that coordinate DNA-based processes including transcription and DNA damage response (DDR) pathways. A major signal involved in these processes is acetylation, which when attached to lysines within proteins, including histones, can be recognized and read by bromodomain-containing proteins. We recently identified the bromodomain protein ZMYND8 (also known as RACK7 and PRKCBP1) as a critical DNA damage response factor involved in regulating transcriptional responses and DNA repair activities at DNA double-strand breaks. Other studies have further defined the molecular details for how ZMYND8 interacts with chromatin and other chromatin modifying proteins to exert its DNA damage response functions. ZMYND8 also plays essential roles in regulating transcription during normal cellular growth, perturbation of which promotes cellular processes involved in cancer initiation and progression. In addition to acetylation, histone methylation and demethylase enzymes have emerged as important regulators of ZMYND8. Here we discuss our current understanding of the molecular mechanisms that govern ZMYND8 function within chromatin, highlighting the importance of this protein for genome maintenance both during the DDR and in cancer.

Indexed as

DNA RepairChromatinDNA Breaks, Double-StrandedHumansMi-2 Nucleosome Remodeling and Deacetylase ComplexNeoplasm MetastasisNeoplasmsProtein Processing, Post-TranslationalRetinoblastoma-Binding Protein 2Signal TransductionTranscription, GeneticTumor Suppressor ProteinsChromatinKDM5A protein, humanMi-2 Nucleosome Remodeling and Deacetylase ComplexRetinoblastoma-Binding Protein 2Tumor Suppressor ProteinsZMYND8 protein, humanBromodomainCancerChromatinDNA damageHistone modificationsZMYND8

Identifiers

PMID29393731
PMCPMC5927707
OpenAlexW2794148770

What OpenQuestion holds

Textmetadata
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.