Evidence map›Paper›PMID 26698648›Full record

ReviewDNA repair2016

Non-canonical actions of mismatch repair.

Gray F Crouse

Abstract readReview
In one paragraph

Review in DNA repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The methylation-independent mismatch repair machinery inMicrobiology (Reading, England) · 2021
    Review
  10. Article
  11. Review
  12. DNA Mismatch Repair and its Role in Huntington's Disease.Journal of Huntington's disease · 2021
    Review
  13. Article
  14. Review
  15. Review
  16. The deaminase APOBEC3B triggers the death of cells lacking uracil DNA glycosylase.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  17. Plant DNA Repair Pathways and Their Applications in Genome Engineering.Methods in molecular biology (Clifton, N.J.) · 2019
    Review
  18. Review
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Gray F CrouseDepartment of Biology, Emory University, Atlanta, GA 30322, USA. Electronic address: gcrouse@emory.edu.
Emory University · US

Funding

Resistance to UV Damage: Role of Gene RegulationP01ES011163 · NIEHS · EMORY UNIVERSITY · PI MARTIN, W DAVID · 2002 to 2012
$12.6M
Cellular Responses to Radiation and Other Types of DamageR01GM080754 · NIGMS · EMORY UNIVERSITY · PI CROUSE, GRAY F. · 2009 to 2012
$1.2M
NIEHS NIH HHS P01 ES011163NIGMS NIH HHS R01 GM080754NIGMS NIH HHS R01 GM80754
6 · The paper itself

Abstract

At the heart of the mismatch repair (MMR) system are proteins that recognize mismatches in DNA. Such mismatches can be mispairs involving normal or damaged bases or insertion/deletion loops due to strand misalignment. When such mispairs are generated during replication or recombination, MMR will direct removal of an incorrectly paired base or block recombination between nonidentical sequences. However, when mispairs are recognized outside the context of replication, proper strand discrimination between old and new DNA is lost, and MMR can act randomly and mutagenically on mispaired DNA. Such non-canonical actions of MMR are important in somatic hypermutation and class switch recombination, expansion of triplet repeats, and potentially in mutations arising in nondividing cells. MMR involvement in damage recognition and signaling is complex, with the end result likely dependent on the amount of DNA damage in a cell.

Indexed as

DNA Mismatch RepairAnimalsBase SequenceDNA ReplicationGene ConversionHumansModels, BiologicalMolecular Sequence DataMutagenesisDNA damageDNA replication fidelityMispaired baseMutagenesisReplicationStrand discrimination

Identifiers

PMID26698648
PMCPMC4740236
OpenAlexW2184785227

What OpenQuestion holds

Textmetadata
LicenceTDM
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.