Evidence map›Paper›PMID 30297842›Full record

ArticleNature communications2018

ATR/Chk1 signaling induces autophagy through sumoylated RhoB-mediated lysosomal translocation of TSC2 after DNA damage.

Mingdong Liu, Taoling Zeng, Xin Zhang, Chunyan Liu, Zhihui Wu, Luming Yao, Changchuan Xie, Hui Xia, Qi Lin, Liping Xie and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 65 citations in OpenAlex.

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  4. International journal of biological sciences · 2026
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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 2 institutions in 2 countries.

Mingdong LiuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Taoling ZengState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Xin ZhangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Chunyan LiuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Zhihui WuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Luming YaoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Changchuan XieState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Hui XiaState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Qi LinState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Liping XieState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Dawang ZhouState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.ORCID http://orcid.org/0000-0002-9053-5249
Xianming DengState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China.
Hong-Lin ChanInstitute of Bioinformatics and Structural Biology, Department of Medical Sciences, National Tsing Hua University, Hsinchu, 30013, Taiwan.
Tong-Jin ZhaoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China. zhaotj@xmu.edu.cn.
Hong-Rui WangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Fujian, 361102, China. wanghr@xmu.edu.cn.
Xiamen University · CNNational Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage can induce autophagy; however, the underlying mechanism remains largely unknown. Here we report that DNA damage leads to autophagy through ATR/Chk1/RhoB-mediated lysosomal recruitment of TSC complex and subsequent mTORC1 inhibition. DNA damage caused by ultraviolet light (UV) or alkylating agent methyl methanesulphonate (MMS) results in phosphorylation of small GTPase RhoB by Chk1. Phosphorylation of RhoB enhances its interaction with the TSC2, and promotes its sumoylation by PIAS1, which is required for RhoB/TSC complex to translocate to lysosomes. As a result, mTORC1 is inhibited, and autophagy is activated. Knockout of RhoB severely attenuates lysosomal translocation of TSC complex and the DNA damage-induced autophagy. Reintroducing wild-type but not sumoylation-resistant RhoB into RhoB

Indexed as

AutophagyDNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsCell Line, TumorCells, CulturedCheckpoint Kinase 1HEK293 CellsHeLa CellsHumansLysosomesMice, KnockoutPhosphorylationProtein TransportrhoB GTP-Binding ProteinRNA InterferenceAtaxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 1CHEK1 protein, humanrhoB GTP-Binding ProteinTSC2 protein, humanTuberous Sclerosis Complex 2 Protein

Identifiers

PMID30297842
PMCPMC6175864
OpenAlexW2895692262

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.