Evidence map›Paper›PMID 39169841›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2024

RAD18- and BRCA1-dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir.

Tasnim Ahmad, Ryotaro Kawasumi, Kouji Hirota

Abstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. RAD18- and BRCA1-dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir.Genes to cells : devoted to molecular & cellular mechanisms · 2024
    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

3 authors.

Tasnim AhmadDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, Tokyo, Japan.
Ryotaro KawasumiDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, Tokyo, Japan.
Kouji HirotaDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, Tokyo, Japan.ORCID https://orcid.org/0000-0003-1676-979X

Funding

Japan Society for the Promotion of Science JP19KK0210Japan Society for the Promotion of Science JP20H04337Japan Society for the Promotion of Science JP21K19235Japan Society for the Promotion of Science JP22K15040Takeda Science FoundationTokyo Metropolitan Government R3-2Yamada Science Foundation
6 · The paper itself

Abstract

Ganciclovir (GCV) is a clinically important drug as it is used to treat viral infections. GCV is incorporated into the DNA during replication, where it interferes with subsequent replication on GCV-incorporated templates. However, the effects of GCV on the host genome and the mechanisms underlying cellular tolerance to GCV remain unclear. In this study, we explored these mechanisms using a collection of mutant DT40 cells. We identified RAD17

Indexed as

BRCA1 ProteinDNA-Binding ProteinsDNA Breaks, Double-StrandedGanciclovirAnimalsAntiviral AgentsCell LineDNA RepairHomologous RecombinationHumansUbiquitin-Protein LigasesAntiviral AgentsBRCA1 ProteinBRCA1 protein, humanDNA-Binding ProteinsGanciclovirRAD18 protein, humanUbiquitin-Protein LigasesBRCA1homologous recombination (HR)nucleoside analogreplicationtemplate switch (TS)

Identifiers

PMID39169841
PMCPMC11555630

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.