Evidence map›Paper›PMID 22101340›Full record

ReviewCell cycle (Georgetown, Tex.)2011

Orchestrating the nucleases involved in DNA interstrand cross-link (ICL) repair.

Blanka Sengerová, Anderson T Wang, Peter J McHugh

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-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

36 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  4. Structure and Function of SNM1 Family Nucleases.Advances in experimental medicine and biology · 2023
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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

3 authors at 1 institution in 1 country.

Blanka SengerováDepartment of Oncology, Weatherall Institute of Molecular Medicine,University of Oxford, John Radcliffe Hospital, Oxford, UK.
Anderson T Wang
Peter J McHugh
John Radcliffe Hospital · GB

Funding

Cancer Research UK
6 · The paper itself

Abstract

DNA interstrand cross-links (ICLs) pose a significant threat to genomic and cellular integrity by blocking essential cellular processes, including replication and transcription. In mammalian cells, much ICL repair occurs in association with DNA replication during S phase, following the stalling of a replication fork at the block caused by an ICL lesion. Here, we review recent work showing that the XPF-ERCC1 endonuclease and the hSNM1A exonuclease act in the same pathway, together with SLX4, to initiate ICL repair, with the MUS81-EME1 fork incision activity becoming important in the absence of the XPF-SNM1A-SLX4-dependent pathway. Another nuclease, the Fanconi anemia-associated nuclease (FAN1), has recently been implicated in the repair of ICLs, and we discuss the possible ways in which the activities of different nucleases at the ICL-stalled replication fork may be coordinated. In relation to this, we briefly speculate on the possible role of SLX4, which contains XPF and MUS81- interacting domains, in the coordination of ICL repair nucleases.

Indexed as

DNA RepairDNA ReplicationAnimalsDNADNA-Binding ProteinsEndodeoxyribonucleasesEndonucleasesEnzyme ActivationExodeoxyribonucleasesFanconi AnemiaHumansMultifunctional EnzymesProtein Structure, TertiaryRecombinasesReplication OriginStructure-Activity RelationshipDNADNA-Binding ProteinsEndodeoxyribonucleasesEndonucleasesERCC1 protein, humanExodeoxyribonucleasesFAN1 protein, humanMultifunctional EnzymesMUS81 protein, humanRecombinasesSLX4 protein, humanxeroderma pigmentosum group F protein

Identifiers

PMID22101340
PMCPMC3272282
OpenAlexW1963569841

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.