Evidence map›Paper›PMID 29017571›Full record

ReviewCell communication and signaling : CCS2017

DNA damage response and cancer therapeutics through the lens of the Fanconi Anemia DNA repair pathway.

Sonali Bhattacharjee, Saikat Nandi

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 92 citations in OpenAlex.

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  15. [Research progress of Fanconi anemia and DNA interstrand crosslink repair].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022
    Article
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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

2 authors at 1 institution in 1 country.

Sonali BhattacharjeeCold Spring Harbor Laboratory, New York, USA. bhattacharjee@cshl.edu.
Saikat NandiCold Spring Harbor Laboratory, New York, USA. snandi@cshl.edu.ORCID 0000-0002-5693-6129
Cold Spring Harbor Laboratory · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fanconi Anemia (FA) is a rare, inherited genomic instability disorder, caused by mutations in genes involved in the repair of interstrand DNA crosslinks (ICLs). The FA signaling network contains a unique nuclear protein complex that mediates the monoubiquitylation of the FANCD2 and FANCI heterodimer, and coordinates activities of the downstream DNA repair pathway including nucleotide excision repair, translesion synthesis, and homologous recombination. FA proteins act at different steps of ICL repair in sensing, recognition and processing of DNA lesions. The multi-protein network is tightly regulated by complex mechanisms, such as ubiquitination, phosphorylation, and degradation signals that are critical for the maintenance of genome integrity and suppressing tumorigenesis. Here, we discuss recent advances in our understanding of how the FA proteins participate in ICL repair and regulation of the FA signaling network that assures the safeguard of the genome. We further discuss the potential application of designing small molecule inhibitors that inhibit the FA pathway and are synthetic lethal with DNA repair enzymes that can be used for cancer therapeutics.

Indexed as

DNA DamageDNA RepairFanconi Anemia Complementation Group ProteinsHumansNeoplasmsSignal TransductionFanconi Anemia Complementation Group ProteinsCancer therapeuticsCombination Therapy Genomic instabilityDNA damage responseDNA repairFanconi Anemia (FA) signaling networkHomologous recombinationInterstrand crosslink (ICL)Synthetic lethalityTranslesion synthesis

Identifiers

PMID29017571
PMCPMC5635482
OpenAlexW2761481949

What OpenQuestion holds

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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.