Evidence map›Paper›PMID 28067825›Full record

ReviewGenes2017

PrimPol-Prime Time to Reprime.

Thomas A Guilliam, Aidan J Doherty

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  7. RAD52 prevents accumulation ofbioRxiv : the preprint server for biology · 2024
    Article
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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

2 authors at 1 institution in 1 country.

Thomas A GuilliamGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton BN1 9RQ, UK. T.Guilliam@sussex.ac.uk.
Aidan J DohertyGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton BN1 9RQ, UK. ajd21@sussex.ac.uk.
University of Sussex · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H019723/1
6 · The paper itself

Abstract

The complex molecular machines responsible for genome replication encounter many obstacles during their progression along DNA. Tolerance of these obstructions is critical for efficient and timely genome duplication. In recent years, primase-polymerase (PrimPol) has emerged as a new player involved in maintaining eukaryotic replication fork progression. This versatile replicative enzyme, a member of the archaeo-eukaryotic primase (AEP) superfamily, has the capacity to perform a range of template-dependent and independent synthesis activities. Here, we discuss the emerging roles of PrimPol as a leading strand repriming enzyme and describe the mechanisms responsible for recruiting and regulating the enzyme during this process. This review provides an overview and update of the current PrimPol literature, as well as highlighting unanswered questions and potential future avenues of investigation.

Indexed as

AEPdamage toleranceDNA replicationpolymeraseprimaseprimingPrimPoltranslesion synthesis

Identifiers

PMID28067825
PMCPMC5295015
OpenAlexW2571288803

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.