Evidence map›Paper›PMID 25520194›Full record

ArticleNucleic acids research2015

RECQL5 and BLM exhibit divergent functions in cells defective for the Fanconi anemia pathway.

Tae Moon Kim, Mi Young Son, Sherry Dodds, Lingchuan Hu, Guangbin Luo, Paul Hasty

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Replication Fork Reversal and Protection.Frontiers in cell 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

6 authors at 3 institutions in 1 country.

Tae Moon KimDepartment of Molecular Medicine and Institute of Biotechnology, The Barshop Center of Aging, University of Texas Health Science Center, San Antonio, TX 78245, USA.
Mi Young SonDepartment of Molecular Medicine and Institute of Biotechnology, The Barshop Center of Aging, University of Texas Health Science Center, San Antonio, TX 78245, USA.
Sherry DoddsDepartment of Molecular Medicine and Institute of Biotechnology, The Barshop Center of Aging, University of Texas Health Science Center, San Antonio, TX 78245, USA.
Lingchuan HuDepartment of Molecular Medicine and Institute of Biotechnology, The Barshop Center of Aging, University of Texas Health Science Center, San Antonio, TX 78245, USA.
Guangbin LuoDepartment of Genetics, Case Western Reserve University, BRB-720, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
Paul HastyDepartment of Molecular Medicine and Institute of Biotechnology, The Barshop Center of Aging, University of Texas Health Science Center, San Antonio, TX 78245, USA hastye@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · USThe University of Texas at San Antonio · USCase Western Reserve University · US

Funding

Cancer Biology Training ProgramT32CA148724 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Pei Wang, Feng-Chun Yang · 2011 to 2026
$3.3M
How does TREX2 maintain and alter chromosomes?R01CA188032 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HASTY, EDWARD PAUL, MONTAGNA, CRISTINA · 2014 to 2018
$1.8M
Study DNA repair in preventing MDS and AML after radiation and benzene exposureR01ES022054 · NIEHS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HASTY, EDWARD PAUL · 2012 to 2016
$1.7M
Discovering TREX1 and TREX2 Function in Mammalian Cells and MiceR01CA123203 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HASTY, EDWARD PAUL · 2007 to 2011
$1.4M
NCI NIH HHS 1 R01 CA123203-01A1NCI NIH HHS R01 CA188032NCI NIH HHS T32 CA148724NIEHS NIH HHS 1 R01 ES022054-01NIEHS NIH HHS R01 ES022054
6 · The paper itself

Abstract

Fanconi anemia (FA) patients exhibit bone marrow failure, developmental defects and cancer. The FA pathway maintains chromosomal stability in concert with replication fork maintenance and DNA double strand break (DSB) repair pathways including RAD51-mediated homologous recombination (HR). RAD51 is a recombinase that maintains replication forks and repairs DSBs, but also rearranges chromosomes. Two RecQ helicases, RECQL5 and Bloom syndrome mutated (BLM) suppress HR through nonredundant mechanisms. Here we test the impact deletion of RECQL5 and BLM has on mouse embryonic stem (ES) cells deleted for FANCB, a member of the FA core complex. We show that RECQL5, but not BLM, conferred resistance to mitomycin C (MMC, an interstrand crosslinker) and camptothecin (CPT, a type 1 topoisomerase inhibitor) in FANCB-defective cells. RECQL5 suppressed, while BLM caused, breaks and radials in FANCB-deleted cells exposed to CPT or MMC, respectively. RECQL5 protected the nascent replication strand from MRE11-mediated degradation and restarted stressed replication forks in a manner additive to FANCB. By contrast BLM restarted, but did not protect, replication forks in a manner epistatic to FANCB. RECQL5 also lowered RAD51 levels in FANCB-deleted cells at stressed replication sites implicating a rearrangement avoidance mechanism. Thus, RECQL5 and BLM impact FANCB-defective cells differently in response to replication stress with relevance to chemotherapeutic regimes.

Indexed as

DNA RepairAnimalsCells, CulturedDNA Breaks, Double-StrandedDNA ReplicationFanconi Anemia Complementation Group ProteinsGene DeletionMiceRecQ HelicasesBloom syndrome proteinFanconi Anemia Complementation Group ProteinsRecQ HelicasesRecql5 protein, mouse

Identifiers

PMID25520194
PMCPMC4333386
OpenAlexW2127283055

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.