Evidence map›Paper›PMID 32649882›Full record

ArticleMolecular cell2020

Tandem Deubiquitination and Acetylation of SPRTN Promotes DNA-Protein Crosslink Repair and Protects against Aging.

Jinzhou Huang, Qin Zhou, Ming Gao, Somaira Nowsheen, Fei Zhao, Wootae Kim, Qian Zhu, Yusuke Kojima, Ping Yin, Yong Zhang and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 51 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

17 authors at 2 institutions in 1 country.

Jinzhou HuangDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Qin ZhouDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Ming GaoDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Somaira NowsheenDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Fei ZhaoDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Wootae KimDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Qian ZhuDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Yusuke KojimaDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Ping YinDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Yong ZhangDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Guijie GuoDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Xinyi TuDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Min DengDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Kuntian LuoDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Bo QinDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Yuichi MachidaDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Zhenkun LouDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: lou.zhenkun@mayo.edu.
Mayo Clinic in Arizona · USMayo Clinic · US

Funding

Regulation of homologous recombination and cancer cell response to chemoradiotherapyR01CA203561 · NCI · MAYO CLINIC ROCHESTER · PI LOU, ZHENKUN · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA203561
6 · The paper itself

Abstract

DNA-protein crosslinks (DPCs) are highly toxic DNA lesions that threaten genomic integrity. Recent findings highlight that SPRTN, a specialized DNA-dependent metalloprotease, is a central player in proteolytic cleavage of DPCs. Previous studies suggest that SPRTN deubiquitination is important for its chromatin association and activation. However, the regulation and consequences of SPRTN deubiquitination remain unclear. Here we report that, in response to DPC induction, the deubiquitinase VCPIP1/VCIP135 is phosphorylated and activated by ATM/ATR. VCPIP1, in turn, deubiquitinates SPRTN and promotes its chromatin relocalization. Deubiquitination of SPRTN is required for its subsequent acetylation, which promotes SPRTN relocation to the site of chromatin damage. Furthermore, Vcpip1 knockout mice are prone to genomic instability and premature aging. We propose a model where two sequential post-translational modifications (PTMs) regulate SPRTN chromatin accessibility to repair DPCs and maintain genomic stability and a healthy lifespan.

Indexed as

DNA RepairAcetylationAgingAnimalsCell LineDeubiquitinating EnzymesDNA-Binding ProteinsDNA DamageEndopeptidasesFemaleGenomic InstabilityHEK293 CellsHumansMaleMice, Inbred C57BLMice, KnockoutDeubiquitinating EnzymesDNA-Binding ProteinsEndopeptidasesSPRTN protein, humanVCPIP1 protein, humanacetylationagingDNA-protein crosslinkDNA repairgenomic instabilitymetalloproteaseSPRTNTop1ccubiquitinationVCPIP1/VCIP135

Identifiers

PMID32649882
PMCPMC7484104
OpenAlexW3041628476

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.