Evidence map›Paper›PMID 20888339›Full record

ArticleJournal of molecular biology2010

Translesion synthesis across abasic lesions by human B-family and Y-family DNA polymerases α, δ, η, ι, κ, and REV1.

Jeong-Yun Choi, Seonhee Lim, Eun-Jin Kim, Ara Jo, F Peter Guengerich

Abstract read
In one paragraph

Article in Journal of molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.2field-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

80 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Frequent Detection of Abasic Sites andChemical research in toxicology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Replication of [AT/TA]Biochemistry · 2024
    Article
  14. The Catalytic Activity of Human REV1 on Undamaged and Damaged DNA.International journal of molecular sciences · 2024
    Article
  15. Review
  16. Replication Bypass of theBiochemistry · 2024
    Article
  17. Article
  18. Replication of [AT/TA]bioRxiv : the preprint server for biology · 2023
    Article
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Jeong-Yun ChoiDepartment of Pharmacology, School of Medicine, Ewha Womans University, 911-1, Mok-5-dong, Yangcheon-gu, Seoul 158-710, Republic of Korea. jychoi@ewha.ac.kr.
Seonhee Lim
Eun-Jin Kim
Ara Jo
F Peter Guengerich
Ewha Womans University · KRVanderbilt University · US

Funding

POLYMERASE INTERACTIONS WITH CARCINOGEN MODIFIED DNAR01ES010375 · NIEHS · VANDERBILT UNIVERSITY · PI GUENGERICH, F PETER · 2000 to 2014
$5.9M
NIEHS NIH HHS R01 ES010375NIEHS NIH HHS R01ES010375
6 · The paper itself

Abstract

Abasic (apurinic/apyrimidinic, AP) sites are the most common DNA lesions formed in cells, induce severe blocks to DNA replication, and are highly mutagenic. Human Y-family translesion DNA polymerases (pols) such as pols η, ι, κ, and REV1 have been suggested to play roles in replicative bypass across many DNA lesions where B-family replicative pols stall, but their individual catalytic functions in AP site bypass are not well understood. In this study, oligonucleotides containing a synthetic abasic lesion (tetrahydrofuran analogue) were compared for catalytic efficiency and base selectivity with human Y-family pols η, ι, κ, and REV1 and B-family pols α and δ. Pol η and pol δ/proliferating cell nuclear antigen (PCNA) copied past AP sites quite effectively and generated products ranging from one-base to full-length extension. Pol ι and REV1 readily incorporated one base opposite AP sites but then stopped. Pols κ and α were severely blocked at AP sites. Pol η preferentially inserted T and A; pol ι inserted T, G, and A; pol κ inserted C and A; REV1 preferentially inserted C opposite AP sites. The B-family pols α and δ/PCNA preferentially inserted A (85% and 58%, respectively) consonant with the A-rule hypothesis. Pols η and δ/PCNA were much more efficient in next-base extension, preferably from A positioned opposite an AP site, than pol κ. These results suggest that AP sites might be bypassed with moderate efficiency by single B- and Y-family pols or combinations, possibly by REV1 and pols ι, η, and δ/PCNA at the insertion step opposite the lesion and by pols η and δ/PCNA at the subsequent extension step. The patterns of the base preferences of human B-family and Y-family pols in both insertion and extension are pertinent to some of the mutagenesis events induced by AP lesions in human cells.

Indexed as

DNA ReplicationDNADNA DamageDNA-Directed DNA PolymeraseDNA Polymerase IDNA Polymerase IIIDNA Polymerase iotaDNA RepairHumansKineticsNuclear ProteinsNucleotidyltransferasesOligonucleotidesProliferating Cell Nuclear AntigenY-Family DNA PolymerasesDNADNA-Directed DNA PolymeraseDNA Polymerase IDNA Polymerase IIIDNA Polymerase iotaNuclear ProteinsNucleotidyltransferasesOligonucleotidesPOLI protein, humanPOLK protein, humanProliferating Cell Nuclear AntigenRad30 proteinREV1 protein, humanY-Family DNA Polymerases

Identifiers

PMID20888339
PMCPMC3018708
OpenAlexW2136581914

What OpenQuestion holds

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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.