Evidence map›Paper›PMID 9288788›Full record

ArticleCancer research1997

Differential involvement of the human mismatch repair proteins, hMLH1 and hMSH2, in transcription-coupled repair.

S A Leadon, A V Avrutskaya

RetractedAbstract readRetracted Publication
PubMed
In one paragraph

Article in Cancer research, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The effect of curcumin on mismatch repair (MMR) proteins hMSH2 and hMLH1 after ultraviolet (UV) irradiation on HL-60 cells.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2003
    Article
  6. Article
  7. Article
  8. Translocation of Cockayne syndrome group A protein to the nuclear matrix: possible relevance to transcription-coupled DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Different mutator phenotypes in Mlh1- versus Pms2-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  16. Review
  17. Microsatellite instability in Drosophila spellchecker1 (MutS homolog) mutants.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  18. Physical interaction between components of DNA mismatch repair and nucleotide excision repair.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

S A LeadonDepartment of Radiation Oncology, University of North Carolina, Chapel Hill 27599-7512, USA.
A V Avrutskaya

Funding

TRANSCRIPTION COUPLED REPAIR OF EUKARYOTIC CELLSR01CA040453 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI LEADON, STEVEN A · 1985 to 2002
$629k
NCI NIH HHS CA40453
6 · The paper itself

Abstract

Defects in DNA mismatch repair have been associated with both hereditary and sporadic forms of cancer. Recently, it has been shown that human cell lines deficient in mismatch repair were also defective in the transcription-coupled repair (TCR) of UV-induced DNA damage. We examined whether TCR of ionizing radiation-induced DNA damage also requires the genes involved in DNA mismatch repair. Cells defective in the hMSH2 gene were deficient in the removal of oxidative damage, including thymine glycols, from the transcribed strand of an active gene. However, an hMLH1 mutant showed normal levels of TCR. By comparison, defects in either hMSH2 or hMLH1 resulted in reduced TCR of UV damage. Introducing chromosomes carrying either hMSH2 or hMLH1 into these cell lines restored their ability to carry out TCR. Deficiencies in either hMSH2 or hMLH1 did not result in decreased overall genomic levels of repair or lead to an increased sensitivity to either UV or ionizing radiation. Our results provide the first evidence for a protein that is absolutely required for the preferential removal of UV-induced DNA damage but not oxidative DNA damage from the transcribed strand of an active human gene.

Indexed as

DNA-Binding ProteinsDNA DamageDNA RepairAdaptor Proteins, Signal TransducingCarrier ProteinsCell SurvivalDNA, NeoplasmHumansMetallothioneinMutationMutL Protein Homolog 1MutS Homolog 2 ProteinNeoplasm ProteinsNuclear ProteinsProto-Oncogene ProteinsThymineAdaptor Proteins, Signal TransducingCarrier ProteinsDNA-Binding ProteinsDNA, NeoplasmMetallothioneinMLH1 protein, humanMSH2 protein, humanMutL Protein Homolog 1MutS Homolog 2 ProteinNeoplasm ProteinsNuclear ProteinsProto-Oncogene ProteinsThyminethymine glycol

Identifiers

PMID9288788

What OpenQuestion holds

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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.