Evidence map›Paper›PMID 18573881›Full record

ArticleMolecular and cellular biology2008

p53-targeted LSD1 functions in repression of chromatin structure and transcription in vivo.

Wen-Wei Tsai, Thi T Nguyen, Yang Shi, Michelle Craig Barton

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.2field-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

42 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Strategies that regulate LSD1 for novel therapeutics.Acta pharmaceutica Sinica. B · 2024
    Review
  3. Role of NADCellular and molecular neurobiology · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. The p53/Adipose-Tissue/Cancer Nexus.Frontiers in endocrinology · 2018
    Review
  10. Simple Maturation of Direct-Converted Hepatocytes Derived from Fibroblasts.Tissue engineering and regenerative medicine · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Epigenetic regulation of EMT: the Snail story.Current pharmaceutical design · 2014
    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

4 authors at 2 institutions in 1 country.

Wen-Wei TsaiDept. of Biochemistry and Molecular Biology, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 1000, Houston, TX 77030, USA.
Thi T Nguyen
Yang Shi
Michelle Craig Barton
The University of Texas MD Anderson Cancer Center · USHarvard University · US

Funding

In Vitro Reconstitution of Alpha Fetroprotein RegulationR01GM053683 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BARTON, MICHELLE ANN · 1997 to 2007
$1.6M
NIGMS NIH HHS GM53683NIGMS NIH HHS R01 GM053683
6 · The paper itself

Abstract

Despite years of study focused on the tumor suppressor p53, little is understood about its functions in normal, differentiated cells. We found that p53 directly interacts with lysine-specific demethylase 1 (LSD1) to alter chromatin structure and confer developmental repression of the tumor marker alpha-fetoprotein (AFP). Chromatin immunoprecipitation (ChIP) and sequential ChIP of developmentally staged liver showed that p53 and LSD1 cooccupy a p53 response element, concomitant with dimethylated histone H3 lysine 4 (H3K4me2) demethylation and postnatal repression of AFP transcription. In p53-null mice, LSD1 binding is depleted, H3K4me2 is increased, and H3K9me2 remains unchanged compared to those of the wild type, underscoring the specificity of p53-LSD1 complexes in demethylation of H3K4me2. We performed partial hepatectomy of wild-type mouse liver and induced a regenerative response, which led to a loss of p53, increased H3K4me2, and decreased LSD1 interaction at AFP chromatin, in parallel with reactivation of AFP expression. In contrast, nuclear translocation of p53 in mouse embryonic fibroblasts led to p53 interaction with p21/CIP1 chromatin, without recruitment of LSD1, and to activation of p21/CIP1. These findings reveal that LSD1 is targeted to chromatin by p53, likely in a gene-specific manner, and define a molecular mechanism by which p53 mediates transcription repression in vivo during differentiation.

Indexed as

Transcription, Geneticalpha-FetoproteinsAnimalsCell LineChromatinCyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, DevelopmentalHepatocytesHistone DemethylasesHumansLiver RegenerationMiceMice, Inbred C57BLOxidoreductases, N-DemethylatingPromoter Regions, GeneticProtein Bindingalpha-FetoproteinsChromatinCyclin-Dependent Kinase Inhibitor p21Histone DemethylasesKDM1a protein, mouseOxidoreductases, N-DemethylatingRepressor ProteinsTumor Suppressor Protein p53

Identifiers

PMID18573881
PMCPMC2519740
OpenAlexW2017188188

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.