Evidence map›Paper›PMID 23042675›Full record

ArticleNucleic acids research2012

Pol β associated complex and base excision repair factors in mouse fibroblasts.

Rajendra Prasad, Jason G Williams, Esther W Hou, Samuel H Wilson

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Topoisomerase I-driven repair of UV-induced damage in NER-deficient cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Review
  12. Article
  13. Review
  14. Two-way crosstalk between BER and c-NHEJ repair pathway is mediated by Pol-β and Ku70.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  15. Damage sensor role of UV-DDB during base excision repair.Nature structural & molecular biology · 2019
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Coordination of DNA single strand break repair.Free radical biology & medicine · 2017
    Review
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

4 authors at 2 institutions in 1 country.

Rajendra PrasadLaboratory of Structural Biology, NIEHS, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA.
Jason G Williams
Esther W Hou
Samuel H Wilson
National Institutes of Health · USNational Institute of Environmental Health Sciences · US

Funding

Protein Microcharacterization ZICES102488 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WILLIAMS, JASON · 2009 to 2025
$19.2M
BIOLOGY OF MAMMALIAN BASE EXCISION REPAIRZ01ES050159 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WILSON, SAMUEL H · 1997 to 2008
$4.5M
Nucleic Acid Enzymes--Pol Beta And Base Repair EnzymesZ01ES050158 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WILSON, SAMUEL H · 1997 to 2008
$2.8M
Intramural NIH HHSNIEHS NIH HHS Z01ES050158NIEHS NIH HHS Z01ES50159
6 · The paper itself

Abstract

During mammalian base excision repair (BER) of lesion-containing DNA, it is proposed that toxic strand-break intermediates generated throughout the pathway are sequestered and passed from one step to the next until repair is complete. This stepwise process is termed substrate channeling. A working model evaluated here is that a complex of BER factors may facilitate the BER process. FLAG-tagged DNA polymerase (pol) β was expressed in mouse fibroblasts carrying a deletion in the endogenous pol β gene, and the cell extract was subjected to an 'affinity-capture' procedure using anti-FLAG antibody. The pol β affinity-capture fraction (ACF) was found to contain several BER factors including polymerase-1, X-ray cross-complementing factor1-DNA ligase III and enzymes involved in processing 3'-blocked ends of BER intermediates, e.g. polynucleotide kinase and tyrosyl-DNA phosphodiesterase 1. In contrast, DNA glycosylases, apurinic/aprymidinic endonuclease 1 and flap endonuclease 1 and several other factors involved in BER were not present. Some of the BER factors in the pol β ACF were in a multi-protein complex as observed by sucrose gradient centrifugation. The pol β ACF was capable of substrate channeling for steps in vitro BER and was proficient in in vitro repair of substrates mimicking a 3'-blocked topoisomerase I covalent intermediate or an oxidative stress-induced 3'-blocked intermediate.

Indexed as

DNA RepairAnimalsCell ExtractsDNADNA ContaminationDNA Polymerase betaDNA Repair EnzymesFibroblastsMicePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesCell ExtractsDNADNA Polymerase betaDNA Repair EnzymesParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerases

Identifiers

PMID23042675
PMCPMC3526277
OpenAlexW1992809685

What OpenQuestion holds

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LicenceCC BY-NC
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.