Evidence map›Paper›PMID 26622943›Full record

ArticleGenes & cancer2015

A novel MeCP2 acetylation site regulates interaction with ATRX and HDAC1.

Somnath Pandey, Glenn E Simmons, Svitlana Malyarchuk, Tara N Calhoun, Kevin Pruitt

Open access · diamondAbstract read
In one paragraph

Article in Genes & cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. The Versatility of Sirtuin-1 in Endocrinology and Immunology.Frontiers in cell and developmental biology · 2020
    Review
  14. Article
  15. Review
  16. Article
  17. 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

5 authors at 3 institutions in 1 country.

Somnath PandeyImmunology and Molecular Microbiology, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Glenn E SimmonsDepartment of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Svitlana MalyarchukMolecular and Cellular Physiology, Shreveport, LA, USA ; LSU Health Sciences Center School of Medicine, Shreveport, LA, USA.
Tara N CalhounMolecular and Cellular Physiology, Shreveport, LA, USA ; LSU Health Sciences Center School of Medicine, Shreveport, LA, USA.
Kevin PruittImmunology and Molecular Microbiology, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Louisiana State University Health Sciences Center Shreveport · USTexas Tech University · USThe University of Texas Southwestern Medical Center · US

Funding

Mechanisms of Epigenetic Gene SilencingR01CA155223 · NCI · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI PRUITT, KEVIN · 2011 to 2015
$1.4M
NCI NIH HHS R01 CA155223
6 · The paper itself

Abstract

Methyl-CpG-binding protein-2 (MeCP2) regulates gene expression by recruiting SWI/SNF DNA helicase/ATPase (ATRX) and Histone Deacetylase-1 (HDAC1) to methylated gene regions and modulates heterochromatin association by interacting with Heterochromatin protein-1. As MeCP2 contributes to tumor suppressor gene silencing and its mutation causes Rett Syndrome, we investigated how novel post-translational-modification contributes to its function. Herein we report that upon pharmacological inhibition of SIRT1 in RKO colon and MCF-7 breast cancer cells, endogenous MeCP2 is acetylated at sites critical for binding to DNA and transcriptional regulators. We created an acetylation mimetic mutation in MeCP2 and found it to possess decreased binding to ATRX and HDAC1. Conditions inducing MeCP2 acetylation do not alter its promoter occupancy at a subset of target genes analyzed, but do cause decreased binding to ATRX and HDAC1. We also report here that a specific inhibitor of SIRT1, IV, can be used to selectively decrease H3K27me3 repressive marks on a subset of repressed target gene promoters analyzed. Lastly, we show that RKO cells over-expressing MeCP2 mutant show reduced proliferation compared to those over-expressing MeCP2-wildtype. Our study demonstrates the importance of acetylated lysine residues and suggests their key role in regulating MeCP2 function and its ability to bind transcriptional regulators.

Indexed as

ATRXepigeneticsHDAC1MeCP2SIRT1

Identifiers

PMID26622943
PMCPMC4633168
OpenAlexW2462163055

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.