Evidence map›Paper›PMID 33963872›Full record

ArticleNucleic acids research2021

NSMF promotes the replication stress-induced DNA damage response for genome maintenance.

Min Kyung Ju, Kyeong Jin Shin, Joo Rak Lee, Keon Woo Khim, Eun A Lee, Jae Sun Ra, Byung-Gyu Kim, Han-Seul Jo, Jong Hyuk Yoon, Tae Moon Kim and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 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

14 authors at 3 institutions in 1 country.

Min Kyung JuDepartment of Life Sciences, Ulsan National University of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.
Kyeong Jin ShinDepartment of Life Sciences, Ulsan National University of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.
Joo Rak LeeDepartment of Life Sciences, Ulsan National University of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.
Keon Woo KhimDepartment of Life Sciences, Ulsan National University of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.
Eun A LeeCenter for Genomic Integrity Institute for Basic Science (IBS), UNIST, Ulsan 44919, Republic of Korea.
Jae Sun RaCenter for Genomic Integrity Institute for Basic Science (IBS), UNIST, Ulsan 44919, Republic of Korea.
Byung-Gyu KimCenter for Genomic Integrity Institute for Basic Science (IBS), UNIST, Ulsan 44919, Republic of Korea.
Han-Seul JoNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu 41062, Republic of Korea.
Jong Hyuk YoonNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu 41062, Republic of Korea.
Tae Moon KimCenter for Genomic Integrity Institute for Basic Science (IBS), UNIST, Ulsan 44919, Republic of Korea.ORCID 0000-0001-9715-9568
Kyungjae MyungCenter for Genomic Integrity Institute for Basic Science (IBS), UNIST, Ulsan 44919, Republic of Korea.
Jang Hyun ChoiDepartment of Life Sciences, Ulsan National University of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.
Hongtae KimDepartment of Life Sciences, Ulsan National University of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.
Young Chan ChaeDepartment of Life Sciences, Ulsan National University of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.ORCID 0000-0002-5869-5250
Institute for Basic Science · KRUlsan National Institute of Science and Technology · KRKorea Brain Research Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proper activation of DNA repair pathways in response to DNA replication stress is critical for maintaining genomic integrity. Due to the complex nature of the replication fork (RF), problems at the RF require multiple proteins, some of which remain unidentified, for resolution. In this study, we identified the N-methyl-D-aspartate receptor synaptonuclear signaling and neuronal migration factor (NSMF) as a key replication stress response factor that is important for ataxia telangiectasia and Rad3-related protein (ATR) activation. NSMF localizes rapidly to stalled RFs and acts as a scaffold to modulate replication protein A (RPA) complex formation with cell division cycle 5-like (CDC5L) and ATR/ATR-interacting protein (ATRIP). Depletion of NSMF compromised phosphorylation and ubiquitination of RPA2 and the ATR signaling cascade, resulting in genomic instability at RFs under DNA replication stress. Consistently, NSMF knockout mice exhibited increased genomic instability and hypersensitivity to genotoxic stress. NSMF deficiency in human and mouse cells also caused increased chromosomal instability. Collectively, these findings demonstrate that NSMF regulates the ATR pathway and the replication stress response network for genome maintenance and cell survival.

Indexed as

DNA DamageDNA RepairAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA ReplicationHEK293 CellsHeLa CellsHumansMiceMice, KnockoutReplication Protein ARNA-Binding ProteinsTranscription FactorsAtaxia Telangiectasia Mutated ProteinsATR protein, humanCDC5L protein, humanCell Cycle ProteinsNSMF protein, humanReplication Protein ARNA-Binding ProteinsRPA2 protein, humanTranscription Factors

Identifiers

PMID33963872
PMCPMC8191778
OpenAlexW3158331288

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.