Evidence map›Paper›PMID 26871286›Full record

ArticleOncotarget2016

Rad18 is required for functional interactions between FANCD2, BRCA2, and Rad51 to repair DNA topoisomerase 1-poisons induced lesions and promote fork recovery.

Kaushlendra Tripathi, Chinnadurai Mani, David W Clark, Komaraiah Palle

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. GermlineJournal of personalized medicine · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Role ofNon-coding RNA research · 2016
    Review
  16. Regulation of DNA repair by non-coding miRNAs.Non-coding RNA research · 2016
    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.

Kaushlendra TripathiDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, 36604, USA.
Chinnadurai ManiDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, 36604, USA.
David W ClarkDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, 36604, USA.
Komaraiah PalleDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, 36604, USA.
USA Mitchell Cancer Institute · USUniversity of South Alabama · US

Funding

Ras18-mediated Fanconi Anemia pathway activation in response to camptothecinR01GM098956 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PALLE, KOMARAIAH · 2012 to 2016
$1.1M
NIGMS NIH HHS R01 GM098956
6 · The paper itself

Abstract

Camptothecin (CPT) and its analogues are chemotherapeutic agents that covalently and reversibly link DNA Topoisomerase I to its nicked DNA intermediate eliciting the formation of DNA double strand breaks (DSB) during replication. The repair of these DSB involves multiple DNA damage response and repair proteins. Here we demonstrate that CPT-induced DNA damage promotes functional interactions between BRCA2, FANCD2, Rad18, and Rad51 to repair the replication-associated DSB through homologous recombination (HR). Loss of any of these proteins leads to equal disruption of HR repair, causes chromosomal aberrations and sensitizes cells to CPT. Rad18 appears to function upstream in this repair pathway as its downregulation prevents activation of FANCD2, diminishes BRCA2 and Rad51 protein levels, formation of nuclear foci of all three proteins and recovery of stalled or collapsed replication forks in response to CPT. Taken together this work further elucidates the complex interplay of DNA repair proteins in the repair of replication-associated DSB.

Indexed as

DNA Breaks, Double-StrandedDNA RepairCamptothecinCell Line, TumorDNA-Binding ProteinsDNA Topoisomerases, Type IFanconi Anemia Complementation Group D2 ProteinHCT116 CellsHumansNeoplasmsRad51 RecombinaseRNA, Small InterferingTransfectionUbiquitin-Protein LigasesCamptothecinDNA-Binding ProteinsDNA Topoisomerases, Type IFANCD2 protein, humanFanconi Anemia Complementation Group D2 ProteinRAD18 protein, humanRAD51 protein, humanRad51 RecombinaseRNA, Small InterferingUbiquitin-Protein LigasesBRCA2DNA topoisomerase 1FANCD2Rad18Rad51

Identifiers

PMID26871286
PMCPMC4914303
OpenAlexW2339416615

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.