Cited by 53Cancer-related Molecular PathwaysGenomics and Chromatin DynamicsEpigenetics and DNA Methylation

p53-mediated heterochromatin reorganization regulates its cell fate decisions.

Open access
Mungamuri, Sathish Kumar, Benson, Erica Kay, Wang, Shaomeng, Gu, Wei, Lee, Sam W, Aaronson, Stuart A·2012·Nature Structural & Molecular Biology

Abstract

p53 is a major sensor of cellular stresses, and its activation influences cell fate decisions. We identified SUV39H1, a histone code 'writer' responsible for the histone H3 Lys9 trimethylation (H3K9me3) mark for 'closed' chromatin conformation, as a target of p53 repression. SUV39H1 downregulation was mediated transcriptionally by p21 and post-translationally by MDM2. The H3K9me3 repression mark was found to be associated with promoters of representative p53 target genes and was decreased upon p53 activation. Overexpression of SUV39H1 maintained higher levels of the H3K9me3 mark on these promoters and was associated with decreased p53 promoter occupancy and decreased transcriptional induction in response to p53. Conversely, SUV39H1 pre-silencing decreased H3K9me3 levels on these promoters and enhanced the p53 apoptotic response. These findings uncover a new layer of p53-mediated chromatin regulation through modulation of histone methylation at p53 target promoters.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nsmb.2271

Cites

60 of 60 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • SUV39H1 negatively regulates p53 transcriptional activation by co-localizing with p53 at target promoters and trimethylating H3K9 to promote heterochromatin.

    “As with Mdm4, SUV39H1 negatively regulates the transcriptional activation of p53. It does so by co-localizing with p53 at the promoters of target genes, where it trimethylates lysine 9 of histone H3 (H3K9me3) to promote formation of transcriptionally inactive higher-order heterochromatin (Mungamuri et al., 2012).”

    From USP7 Is a Master Regulator of Genome Stability (2020) · cites this paper as Mungamuri et al., 2012

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Mungamuri, S. K., Benson, E. K., Wang, S., Gu, W., Lee, S. W., & Aaronson, S. A.
Affiliations
  • Icahn School of Medicine at Mount Sinai (US)
  • University of Michigan (US)
  • Columbia University (US)
  • Harvard University (US)
Corresponding author
Aaronson, Stuart A
Venue
Nature Structural & Molecular Biology
Published
2012-04-01
Volume
19
Issue
5
Pages
478-484
ISSN
  • 1545-9985 (ISSN-L)
  • 1545-9993
OpenAlex
W2157049798
Cited by
53
References
60
Citations by year
2026: 1 · 2025: 4 · 2024: 1 · 2023: 5 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 4 · 2015: 4 · 2014: 7 · 2013: 8 · 2012: 1
FWCI
3.16
Type
journal article
Language
en
Open access
Locations
  • Nature Structural & Molecular Biology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (2r01ca085533-16)
  • National Cancer Institute (R01-CA085533, P01CA080058)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords
p53, SUV39H1, H3K9me3, heterochromatin, histone methylation, p21, MDM2, chromatin regulation, cell fate determination, apoptosis, transcriptional repression
MeSH terms
Cell Line, Gene Expression Regulation, Heterochromatin, Histones, Humans, Methylation, Methyltransferases, Repressor Proteins, Tumor Suppressor Protein p53, Apoptosis, Cyclin-Dependent Kinase Inhibitor p21, Proto-Oncogene Proteins c-mdm2, Cell Cycle Checkpoints

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review