Evidence map›Paper›PMID 20231313›Full record

ArticleGenes & development2010

{Delta}Np73{beta} puts the brakes on DNA repair.

Emma Vernersson-Lindahl, Alea A Mills

Abstract readComment
In one paragraph

Article in Genes & development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Emma Vernersson-LindahlCold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
Alea A Mills

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian cells are barraged with endogenous metabolic byproducts and environmental insults that can lead to nearly a million genomic lesions per cell per day. Networks of proteins that repair these lesions are essential for genome maintenance, and a compromise in these pathways propagates mutations that can cause aging and cancer. The p53 tumor suppressor plays a central role in repairing the effects of DNA damage, and has therefore earned the title of "guardian of the genome." In this issue of Genes & Development, Wilhelm and colleagues (pp. 549-560) demonstrate that p73-an older sibling of p53-inhibits pathways that resolve DNA double-strand breaks.

Indexed as

AnimalsCellular SenescenceDisease Models, AnimalDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairHumansNeoplasmsNuclear ProteinsTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteinsdelta Np73 protein, humanDNA-Binding ProteinsNuclear ProteinsTP73 protein, humanTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID20231313
PMCPMC2841329

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.