Evidence map›Paper›PMID 35271816›Full record

ArticleMolecular cell2022

Active DNA damage eviction by HLTF stimulates nucleotide excision repair.

Marvin van Toorn, Yasemin Turkyilmaz, Sueji Han, Di Zhou, Hyun-Suk Kim, Irene Salas-Armenteros, Mihyun Kim, Masaki Akita, Franziska Wienholz, Anja Raams and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.4field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 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

21 authors at 5 institutions in 3 countries.

Marvin van ToornDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Yasemin TurkyilmazDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Sueji HanCenter for Bioanalysis, Korea Research Institute of Standards and Science, Daejeon 305-340, Republic of Korea; Department of Bio-Analytical Science, University of Science & Technology, Daejeon 305-350, Republic of Korea.
Di ZhouDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Hyun-Suk KimCenter for Genomic Integrity, Institute for Basic Science, Ulsan 44919, Republic of Korea.
Irene Salas-ArmenterosDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Mihyun KimCenter for Genomic Integrity, Institute for Basic Science, Ulsan 44919, Republic of Korea; Department of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Masaki AkitaDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Franziska WienholzDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Anja RaamsDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Eunjin RyuCenter for Genomic Integrity, Institute for Basic Science, Ulsan 44919, Republic of Korea; Department of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Sukhyun KangCenter for Genomic Integrity, Institute for Basic Science, Ulsan 44919, Republic of Korea.
Arjan F TheilDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Karel BezstarostiProteomics Centre, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Maria TresiniDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Giuseppina Giglia-MariInstitut NeuroMyoGène (INMG), CNRS UMR 5310, INSERM U1217, Université de Lyon, Université Claude Bernard Lyon1, 16 rue Dubois, 69622 Villeurbanne Cedex, France.
Jeroen A DemmersProteomics Centre, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Orlando D SchärerCenter for Genomic Integrity, Institute for Basic Science, Ulsan 44919, Republic of Korea; Department of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Jun-Hyuk ChoiCenter for Bioanalysis, Korea Research Institute of Standards and Science, Daejeon 305-340, Republic of Korea; Department of Bio-Analytical Science, University of Science & Technology, Daejeon 305-350, Republic of Korea.
Wim VermeulenDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands.
Jurgen A MarteijnDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Centre, Rotterdam, the Netherlands. Electronic address: j.marteijn@erasmusmc.nl.
Oncode Institute · NLInstitute for Basic Science · KRErasmus University Rotterdam · NLKorea Research Institute of Standards and Science · KRUniversité Claude Bernard Lyon 1 · FR

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
NCI NIH HHS P01 CA092584
6 · The paper itself

Abstract

Nucleotide excision repair (NER) counteracts the onset of cancer and aging by removing helix-distorting DNA lesions via a "cut-and-patch"-type reaction. The regulatory mechanisms that drive NER through its successive damage recognition, verification, incision, and gap restoration reaction steps remain elusive. Here, we show that the RAD5-related translocase HLTF facilitates repair through active eviction of incised damaged DNA together with associated repair proteins. Our data show a dual-incision-dependent recruitment of HLTF to the NER incision complex, which is mediated by HLTF's HIRAN domain that binds 3'-OH single-stranded DNA ends. HLTF's translocase motor subsequently promotes the dissociation of the stably damage-bound incision complex together with the incised oligonucleotide, allowing for an efficient PCNA loading and initiation of repair synthesis. Our findings uncover HLTF as an important NER factor that actively evicts DNA damage, thereby providing additional quality control by coordinating the transition between the excision and DNA synthesis steps to safeguard genome integrity.

Indexed as

DNA-Binding ProteinsDNA RepairDNADNA DamageDNA ReplicationDNADNA-Binding Proteinsdamage evictionDNA damagegenome stabilityHLTFnucleotide excision repairpost-replication repairrepair synthesisTFIIHUV damage response

Identifiers

PMID35271816
PMCPMC9473497
OpenAlexW4220930914

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.