Evidence map›Paper›PMID 32307824›Full record

ArticleEMBO reports2020

HMCES safeguards replication from oxidative stress and ensures error-free repair.

Mrinal Srivastava, Dan Su, Huimin Zhang, Zhen Chen, Mengfan Tang, Litong Nie, Junjie Chen

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Mrinal SrivastavaDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Dan SuDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0003-1468-3538
Huimin ZhangDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0001-8987-6014
Zhen ChenDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mengfan TangDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Litong NieDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Junjie ChenDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0002-1493-2189
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
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
Fanconi anemia pathway in DNA damage repairR01CA157448 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CHEN, JUNJIE · 2012 to 2016
$1.6M
Enzymatic and Motor Properties of Myosin 19K01CA160667 · NCI · UNIVERSITY OF RICHMOND · PI QUINTERO-CARMONA, OMAR ALBERTO · 2011 to 2013
$353k
Cancer Prevention & Research Institute of Texas RP160667HHS|NIH|National Cancer Institute (NCI) CA157448HHS|NIH|National Cancer Institute (NCI) CA193124HHS|NIH|National Cancer Institute (NCI) P30CA016672NCI NIH HHS P01 CA193124NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA157448
6 · The paper itself

Abstract

Replication across oxidative DNA lesions can give rise to mutations that pose a threat to genome integrity. How such lesions, which escape base excision repair, get removed without error during replication remains unknown. Our PCNA-based screen to uncover changes in replisome composition under different replication stress conditions had revealed a previously unknown PCNA-interacting protein, HMCES/C3orf37. Here, we show that HMCES is a critical component of the replication stress response, mainly upon base misincorporation. We further demonstrate that the absence of HMCES imparts resistance to pemetrexed treatment due to error-prone bypass of oxidative damage. Furthermore, based on genetic screening, we show that homologous recombination repair proteins, such as CtIP, BRCA2, BRCA1, and PALB2, are indispensable for the survival of HMCES KO cells. Hence, HMCES, which is the sole member of the SRAP superfamily in higher eukaryotes known so far, acts as a proofreader on replication forks, facilitates resolution of oxidative base damage, and therefore ensures faithful DNA replication.

Indexed as

DNA RepairDNA ReplicationDNA-Binding ProteinsDNA DamageHEK293 CellsHumansOxidative StressDNA-Binding ProteinsHMCES protein, humanantimetabolite inhibitorsbase excision repairoxidative damagereplication stresstranslesion synthesis

Identifiers

PMID32307824
PMCPMC7271331
OpenAlexW3016804241

What OpenQuestion holds

Textmetadata
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.