Evidence map›Paper›PMID 30018112›Full record

ArticlemBio2018

The Main Role of Srs2 in DNA Repair Depends on Its Helicase Activity, Rather than on Its Interactions with PCNA or Rad51.

Alex Bronstein, Lihi Gershon, Gilad Grinberg, Elisa Alonso-Perez, Martin Kupiec

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in mBio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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 1 institution in 1 country.

Alex BronsteinSchool of Molecular Cell Biology and Biotechnology, Tel Aviv University, Ramat Aviv, Israel.
Lihi GershonSchool of Molecular Cell Biology and Biotechnology, Tel Aviv University, Ramat Aviv, Israel.
Gilad GrinbergSchool of Molecular Cell Biology and Biotechnology, Tel Aviv University, Ramat Aviv, Israel.
Elisa Alonso-PerezSchool of Molecular Cell Biology and Biotechnology, Tel Aviv University, Ramat Aviv, Israel.
Martin KupiecSchool of Molecular Cell Biology and Biotechnology, Tel Aviv University, Ramat Aviv, Israel martin@post.tau.ac.il.
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homologous recombination (HR) is a mechanism that repairs a variety of DNA lesions. Under certain circumstances, however, HR can generate intermediates that can interfere with other cellular processes such as DNA transcription or replication. Cells have therefore developed pathways that abolish undesirable HR intermediates. The

Indexed as

Cell CycleDNA DamageDNA HelicasesDNA RepairDNA ReplicationEnzyme ActivationHomologous RecombinationProliferating Cell Nuclear AntigenRad51 RecombinaseSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSequence DeletionDNA HelicasesPOL30 protein, S cerevisiaeProliferating Cell Nuclear AntigenRAD51 protein, S cerevisiaeRad51 RecombinaseSaccharomyces cerevisiae ProteinsSRS2 protein, S cerevisiaeDNA recombinationDNA repairgenome stabilityPCNARad51Srs2yeasts

Identifiers

PMID30018112
PMCPMC6050964
OpenAlexW2883578253

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.