Evidence map›Paper›PMID 14757832›Full record

ArticleNucleic acids research2004

Poly(ADP-ribose) polymerase (PARP-1) and p53 independently function in regulating double-strand break repair in primate cells.

Silke Süsse, Claus-Jürgen Scholz, Alexander Bürkle, Lisa Wiesmüller

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  5. Mitochondrial Quality Control in Age-Related Pulmonary Fibrosis.International journal of molecular sciences · 2020
    Review
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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 1 institution in 1 country.

Silke SüsseUniversitätsfrauenklinik, Prittwitzstrasse 43, D-89075 Ulm, Germany.
Claus-Jürgen Scholz
Alexander Bürkle
Lisa Wiesmüller
Universitäts Frauenklinik · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PARP-1 is rapidly activated by DNA strand breaks, which finally leads to the modulation of multiple protein activities in DNA replication, DNA repair and checkpoint control. PARP-1 may be involved in homologous recombination, and poly(ADP-ribosyl)ation of p53 represents one possible mechanism that activates p53 as a recombination surveillance factor. Here, we examined the influence of PARP-1 on homology-directed double-strand break (DSB) repair by use of a fluorescence- and I-SceI- meganuclease-based assay with either episomal or chromosomally integrated DNA substrates. Surprisingly, the transient expression of both full-length PARP-1 and of a dominant negative mutant, retaining the DNA-binding but lacking the catalytic domain, down-regulated DSB repair in a dose-dependent manner. This effect was seen regardless of p53 status, however, with enhanced inhibition in the presence of wild-type p53. Taken together, our data reveal that PARP-1 overexpression counteracts DSB repair independently of its enzymatic activity and of poly(ADP-ribosyl)ation of p53 in particular, but synergizes with p53 in suppressing chromosomal rearrangements.

Indexed as

DNA DamageDNA RepairAnimalsCaspase InhibitorsCaspasesCell LineChromosome AberrationsDNAHumansK562 CellsMacaca mulattaPoly(ADP-ribose) PolymerasesProtein BindingRecombination, GeneticSubstrate SpecificityTransfectionCaspase InhibitorsCaspasesDNAPoly(ADP-ribose) PolymerasesTumor Suppressor Protein p53

Identifiers

PMID14757832
PMCPMC373350
OpenAlexW2117258496

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.