Evidence map›Paper›PMID 19838051›Full record

ArticleEpigenetics2009

p53 sumoylation: mechanistic insights from reconstitution studies.

Shwu-Yuan Wu, Cheng-Ming Chiang

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Targeting Moonlighting Enzymes in Cancer.Molecules (Basel, Switzerland) · 2024
    Review
  5. Review
  6. The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution.

Shwu-Yuan WuSimmons Comprehensive Cancer Center and Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Cheng-Ming Chiang
Harold C. Simmons Comprehensive Cancer Center

Funding

E2-Cellular Complexes in HPV Chromatin TranscriptionR01CA103867 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHIANG, CHENG-MING · 2004 to 2017
$4.0M
Regulation of p53 Transcription by Viral Oncoproteins & Covalent ModificationsR01CA124760 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHIANG, CHENG-MING · 2007 to 2012
$1.6M
NCI NIH HHS CA103867NCI NIH HHS CA124760NCI NIH HHS R01 CA103867NCI NIH HHS R01 CA124760
6 · The paper itself

Abstract

Sumoylation represents a cascade of enzymatic reactions mediated by SUMO-activating enzyme (SAE1/SAE2 heterodimer), SUMO-conjugating enzyme Ubc9, and SUMO E3 ligases that include five protein inhibitors of activated STATs (PIAS1, PIAS3, PIASy, PIASxalpha and PIASxbeta), and culminates in the formation of an isopeptide bond between the C-terminal glycine of a small ubiquitin-related modifier (SUMO) and the lysine residue of a protein substrate. Conjugation of a SUMO moiety, ranging from 92 (for SUMO-2) to 97 (for SUMO-1) amino acids, not only increases the molecular size but also alters the property and function of the modified protein. Although sumoylation has been observed with many cellular proteins and the majority of transcription factors including the p53 tumor suppressor, this covalent modification is normally detectable only in a small population, often less than 5%, of a given substrate in vivo. This low abundance of SUMO-modified proteins, due to the presence of sentrin/SUMO-specific proteases (SENPs) that actively cleave the reversible SUMO linkage, has posed a challenge to define the biological effect of SUMO in living cells. Nevertheless, the recent development of reconstituted modification and chromatin-dependent transcription assays has provided unique insights into the molecular action of SUMO in modifying protein function. The availability of these reconstitution systems has unraveled the interplay between sumoylation and acetylation in regulating the DNA binding and transcriptional activity of p53 tetramers and further allow the identification of transcriptional corepressors, such as mSin3A, CoREST1/LSD1 and Mi-2/NuRD implicated in SUMO-dependent gene silencing events.

Indexed as

AnimalsChromatinEpigenesis, GeneticHumansProtein BindingSUMO-1 ProteinTranscription, GeneticTumor Suppressor Protein p53ChromatinSUMO-1 ProteinTumor Suppressor Protein p53

Identifiers

PMID19838051
PMCPMC4749140
OpenAlexW1993759147

What OpenQuestion holds

Textmetadata
LicenceTDM
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.