Evidence map›Paper›PMID 20400978›Full record

ArticleOncogene2010

Role of SUMO:SIM-mediated protein-protein interaction in non-homologous end joining.

Y-J Li, J M Stark, D J Chen, D K Ann, Y Chen

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
  6. Article
  7. Review
  8. Article
  9. OncogeneAmerican journal of cancer research · 2020
    Article
  10. Article
  11. Article
  12. SUMO, a small, but powerful, regulator of double-strand break repair.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  13. Article
  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

5 authors at 3 institutions in 1 country.

Y-J LiDepartment of Molecular Medicine, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.
J M Stark
D J Chen
D K Ann
Y Chen
City of Hope · USCity Of Hope National Medical Center · USRadiation Oncology Associates · US

Funding

SUMO modification and DNA damage response in cancer therapyR01GM086171 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, YUAN · 2008 to 2020
$5.2M
Roles of DNA PK in DNA Double Strand Break RepairR37CA050519 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHEN, DAVID J · 2003 to 2011
$3.5M
Molecular Hierarchies in Salivary Adaptive ResponsesR01DE014183 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANN, DAVID K. · 2001 to 2011
$3.3M
Mechanistic steps of homologous repair in mammalian cellsR01CA120954 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI STARK, JEREMY MICHAEL · 2006 to 2016
$2.2M
The Enzymatic Pathway of a Ubiquitin-Like ModificationR01GM074748 · NIGMS · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI CHEN, YUAN · 2007 to 2010
$1.5M
The role of SUMO-dependent protein protein interaction in DNA double strand breakF32CA134180 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI LI, YI-JIA · 2008 to 2010
$137k
NCI NIH HHS F32 CA134180NCI NIH HHS F32CA134180NCI NIH HHS R01 CA120954NCI NIH HHS R01CA120954NCI NIH HHS R37 CA050519NCI NIH HHS R37CA050519-20NIDCR NIH HHS R01 DE014183NIDCR NIH HHS R01DE14183NIGMS NIH HHS R01 GM074748NIGMS NIH HHS R01GM074748NIGMS NIH HHS R01 GM086171NIGMS NIH HHS R01GM086171
6 · The paper itself

Abstract

Although post-translational modifications by the small ubiquitin-like modifiers (SUMO) are known to be important in DNA damage response, it is unclear whether they have a role in double-strand break (DSB) repair by non-homologous end joining (NHEJ). Here, we analyzed various DSB repair pathways upon inhibition of SUMO-mediated protein-protein interactions using peptides that contain the SUMO-interaction motif (SIM) and discriminate between mono- and SUMO-chain modifications. The SIM peptides specifically inhibit NHEJ as shown by in vivo repair assays and radio-sensitivity of cell lines deficient in different DSB repair pathways. Furthermore, mono-SUMO, instead of SUMO-chain, modifications appear to be involved in NHEJ. Immunoprecipitation experiments also showed that the SIM peptide interacted with SUMOylated Ku70 after radiation. This study is the first to show an important role for SUMO:SIM-mediated protein-protein interactions in NHEJ, and provides a mechanistic basis for the role of SIM peptide in sensitizing genotoxic stress of cancer cells.

Indexed as

DNA RepairAmino Acid MotifsBiomimetic MaterialsCell Line, TumorDNA Breaks, Double-StrandedDNA DamageHumansNeoplasmsPeptidesProtein BindingRadiation ToleranceSequence Homology, Amino AcidSUMO-1 ProteinPeptidesSUMO-1 Protein

Identifiers

PMID20400978
PMCPMC2891878
OpenAlexW2087786655

What OpenQuestion holds

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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.