Evidence map›Paper›PMID 31067464›Full record

ArticleCell reports2019

Remodeling of Interstrand Crosslink Proximal Replisomes Is Dependent on ATR, FANCM, and FANCD2.

Jing Huang, Jing Zhang, Marina A Bellani, Durga Pokharel, Julia Gichimu, Ryan C James, Himabindu Gali, Chen Ling, Zhijiang Yan, Dongyi Xu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 61 citations in OpenAlex.

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  9. Induction of the humanMolecular medicine reports · 2024
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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

15 authors at 7 institutions in 2 countries.

Jing HuangInstitute of Chemical Biology and Nanomedicine, State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Biology, Hunan University, Changsha 410082, China. Electronic address: huangjing16@hnu.edu.cn.
Jing ZhangLaboratory of Molecular Gerontology, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Marina A BellaniLaboratory of Molecular Gerontology, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Durga PokharelLaboratory of Molecular Gerontology, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Julia GichimuLaboratory of Molecular Gerontology, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Ryan C JamesLaboratory of Molecular Gerontology, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Himabindu GaliDepartment of Pharmacology & Experimental Therapeutics and Medicine, Boston University School of Medicine, 72 East Concord St., K-712D, Boston, MA 02118-2526.
Chen LingLaboratory of Genetics and Genomics, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Zhijiang YanInstitute of DNA Repair Diseases, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Dongyi XuPeking University, Beijing 100871, China.
Junjie ChenDepartment Experimental Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77225-0334, USA.
Amom Ruhikanta MeeteiDivision of Experimental Hematology and Cancer Biology and Cancer & Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Lei LiDepartment Experimental Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77225-0334, USA.
Weidong WangLaboratory of Genetics and Genomics, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Michael M SeidmanLaboratory of Molecular Gerontology, National Institute on Aging, NIH, 251 Bayview Blvd., Baltimore, MD 21224, USA. Electronic address: seidmanm@grc.nia.nih.gov.
National Institute on Aging · USThe University of Texas MD Anderson Cancer Center · USBoston University · USCincinnati Children's Hospital Medical Center · USPeking University · CNState Key Laboratory of Chemobiosensing and ChemometricsWenzhou Medical University · CN

Funding

Repair of localized DNA damageZIAAG000746 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL · 2009 to 2025
$30.0M
Project 4: Coordinating Nucleolytic Pathways During Crosslink RepairP01CA193124 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WOOD, RICHARD D · 2017 to 2022
$9.6M
Investigate the DNA damage response pathway of Fanconi anemia and BRCA proteinsZIAAG000688 · NIA · NATIONAL INSTITUTE ON AGING · PI WANG, WEIDONG · 2009 to 2025
$6.9M
Genetic Framework and Molecular Mechanism of Fanconi AnemiaR01CA190635 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, LEI · 2015 to 2018
$1.5M
Factors that modulate cellular homeostasis to overcome replicative stress in agingZIAAG000577 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL · 2017 to 2021
$974k
Repair of localized DNA damageZ01AG000746 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL · 2007 to 2008
$607k
Intramural NIH HHS Z01 AG000746Intramural NIH HHS Z99 AG999999NCI NIH HHS P01 CA193124NCI NIH HHS R01 CA190635NIA NIH HHS Z01 AG000746
6 · The paper itself

Abstract

Eukaryotic replisomes are driven by the mini chromosome maintenance (MCM [M]) helicase complex, an offset ring locked around the template for leading strand synthesis by CDC45 (C) and GINS (G) proteins. Although the CDC45 MCM GINS (CMG) structure implies that interstrand crosslinks (ICLs) are absolute blocks to replisomes, recent studies indicate that cells can restart DNA synthesis on the side of the ICL distal to the initial encounter. Here, we report that restart requires ATR and is promoted by FANCD2 and phosphorylated FANCM. Following introduction of genomic ICLs and dependent on ATR and FANCD2 but not on the Fanconi anemia core proteins or FAAP24, FANCM binds the replisome complex, with concomitant release of the GINS proteins. In situ analysis of replisomes proximal to ICLs confirms the ATR-dependent release of GINS proteins while CDC45 is retained on the remodeled replisome. The results demonstrate the plasticity of CMG composition in response to replication stress.

Indexed as

DNA-Directed DNA PolymeraseMultienzyme ComplexesAnimalsAtaxia Telangiectasia Mutated ProteinsChickensDNA HelicasesDNA ReplicationEpistasis, GeneticFanconi Anemia Complementation Group D2 ProteinFemaleHeLa CellsHumansMaleMiceMultiprotein ComplexesPhosphorylationAtaxia Telangiectasia Mutated ProteinsATR protein, humanDNA-Directed DNA PolymeraseDNA HelicasesFANCD2 protein, humanFANCM protein, humanFanconi Anemia Complementation Group D2 ProteinMultienzyme ComplexesMultiprotein ComplexesReplisomesATRCMGFANCD2FANCMGINSICLinterstrand crosslinkreplication traverse

Identifiers

PMID31067464
PMCPMC6676478
OpenAlexW2944257163

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.