Evidence map›Paper›PMID 32877700›Full record

ReviewProgress in biophysics and molecular biology2020

Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.

Cody M Rogers, Robert H Simmons Iii, Gabriella E Fluhler Thornburg, Nicholas J Buehler, Matthew L Bochman

Open access · greenAbstract readReview
In one paragraph

Review in Progress in biophysics and molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

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  19. Overcoming stochastic variations in culture variables to quantify and compare growth curve data.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021
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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 1 institution in 1 country.

Cody M RogersMolecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA.
Robert H Simmons IiiMolecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA.
Gabriella E Fluhler ThornburgMolecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA.
Nicholas J BuehlerMolecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA.
Matthew L BochmanMolecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA. Electronic address: bochman@indiana.edu.
Indiana University Bloomington · US

Funding

DNA helicases and associated factors in genome stabilityR35GM133437 · NIGMS · TRUSTEES OF INDIANA UNIVERSITY · PI BOCHMAN, MATTHEW LINNE · 2019 to 2023
$2.4M
NIGMS NIH HHS R35 GM133437
6 · The paper itself

Abstract

DNA inter-strand crosslinks (ICLs) are dangerous lesions that can be caused by a variety of endogenous and exogenous bifunctional compounds. Because covalently linking both strands of the double helix locally disrupts DNA replication and transcription, failure to remove even a single ICL can be fatal to the cell. Thus, multiple ICL repair pathways have evolved, with the best studied being the canonical Fanconi anemia (FA) pathway. However, recent research demonstrates that different types of ICLs (e.g., backbone distorting vs. non-distorting) can be discriminated by the cell, which then mounts a specific repair response using the FA pathway or one of a variety of FA-independent ICL repair pathways. This review focuses on the latter, covering current work on the transcription-coupled, base excision, acetaldehyde-induced, and SNM1A/RecQ4 ICL repair pathways and highlighting unanswered questions in the field. Answering these questions will provide mechanistic insight into the various pathways of ICL repair and enable ICL-inducing agents to be more effectively used as chemotherapeutics.

Indexed as

AcetaldehydeAnimalsAntineoplastic AgentsChemistry, PharmaceuticalCross-Linking ReagentsDNADNA-Binding ProteinsDNA DamageDNA RepairDNA ReplicationEndodeoxyribonucleasesFanconi AnemiaHumansMiceMutagenesisNeoplasmsAcetaldehydeAntineoplastic AgentsCross-Linking ReagentsDNADNA-Binding ProteinsEndodeoxyribonucleasesDNA helicaseDNA inter-Strand crosslink repairFanconi anemiaHrq1NucleasePso2

Identifiers

PMID32877700
PMCPMC8201522
OpenAlexW3081552670

What OpenQuestion holds

Textmetadata
LicenceTDM
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.