Evidence map›Paper›PMID 32161327›Full record

ArticleCommunications biology2020

Nuclear myosin 1 activates p21 gene transcription in response to DNA damage through a chromatin-based mechanism.

Tomas Venit, Khairunnisa Semesta, Sannia Farrukh, Martin Endara-Coll, Robert Havalda, Pavel Hozak, Piergiorgio Percipalle

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  9. Article
  10. Article
  11. Myosin in chromosome organisation and gene expression.Biochemical Society transactions · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Regulation of Nuclear Mechanics and the Impact on DNA Damage.International journal of molecular sciences · 2021
    Review
  17. Review
  18. 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

7 authors at 4 institutions in 5 countries.

Tomas VenitScience Division, Biology Program, New York University Abu Dhabi (NYUAD), P.O. Box, 129188, Abu Dhabi, UAE.
Khairunnisa SemestaScience Division, Biology Program, New York University Abu Dhabi (NYUAD), P.O. Box, 129188, Abu Dhabi, UAE.ORCID http://orcid.org/0000-0001-8941-1399
Sannia FarrukhScience Division, Biology Program, New York University Abu Dhabi (NYUAD), P.O. Box, 129188, Abu Dhabi, UAE.
Martin Endara-CollScience Division, Biology Program, New York University Abu Dhabi (NYUAD), P.O. Box, 129188, Abu Dhabi, UAE.ORCID http://orcid.org/0000-0002-7656-2929
Robert HavaldaDepartment of Biology of the Cell Nucleus, Institute of Molecular Genetics, AS CR, v.v.i., Videnska 1083, 142 20, Prague, Czech Republic.
Pavel HozakDepartment of Biology of the Cell Nucleus, Institute of Molecular Genetics, AS CR, v.v.i., Videnska 1083, 142 20, Prague, Czech Republic.
Piergiorgio PercipalleScience Division, Biology Program, New York University Abu Dhabi (NYUAD), P.O. Box, 129188, Abu Dhabi, UAE. pp69@nyu.edu.
New York University · USInstitute of Molecular Genetics · RUNew York University Abu Dhabi · AEStockholm University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear myosin 1 (NM1) has been implicated in key nuclear functions. Together with actin, it has been shown to initiate and regulate transcription, it is part of the chromatin remodeling complex B-WICH, and is responsible for rearrangements of chromosomal territories in response to external stimuli. Here we show that deletion of NM1 in mouse embryonic fibroblasts leads to chromatin and transcription dysregulation affecting the expression of DNA damage and cell cycle genes. NM1 KO cells exhibit increased DNA damage and changes in cell cycle progression, proliferation, and apoptosis, compatible with a phenotype resulting from impaired p53 signaling. We show that upon DNA damage, NM1 forms a complex with p53 and activates the expression of checkpoint regulator p21 (Cdkn1A) by PCAF and Set1 recruitment to its promoter for histone H3 acetylation and methylation. We propose a role for NM1 in the transcriptional response to DNA damage response and maintenance of genome stability.

Indexed as

Chromatin Assembly and DisassemblyDNA DamageTranscription, GeneticAnimalsApoptosisCell CycleCell LineCell NucleusCell ProliferationCyclin-Dependent Kinase Inhibitor p21Epigenesis, GeneticEtoposideHistone-Lysine N-MethyltransferaseMiceMyosin Type Ip300-CBP-Associated FactorCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21EtoposideHistone-Lysine N-MethyltransferaseMyo1c protein, mouseMyosin Type INsccn1 protein, mousep300-CBP-Associated Factorp300-CBP Transcription FactorsTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID32161327
PMCPMC7066169
OpenAlexW3011807702

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.