Evidence map›Paper›PMID 31210753›Full record

ArticleCancer cell international2019

DNA damage-induced activation of ATM promotes β-TRCP-mediated ARID1A ubiquitination and destruction in gastric cancer cells.

Zhou-Hua Jiang, Tao Peng, Hai-Long Qian, Cai-de Lu, Feng Qiu, Su-Zhan Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular 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

6 authors at 3 institutions in 1 country.

Zhou-Hua Jiang1Zhejiang University School of Medicine, Hangzhou, 310009 Zhejiang China.
Tao PengDepartment of Gastrointestinal Surgery, Ningbo Medical Center, Li Huili Eastern Hospital, Ningbo, 315000 Zhejiang China.
Hai-Long QianDepartment of Gastrointestinal Surgery, Ningbo Medical Center, Li Huili Eastern Hospital, Ningbo, 315000 Zhejiang China.
Cai-de LuDepartment of Gastrointestinal Surgery, Ningbo Medical Center, Li Huili Eastern Hospital, Ningbo, 315000 Zhejiang China.
Feng QiuDepartment of Gastrointestinal Surgery, Ningbo Medical Center, Li Huili Eastern Hospital, Ningbo, 315000 Zhejiang China.
Su-Zhan Zhang3Department of Surgical Oncology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009 Zhejiang China.
Ningbo Medical Center Lihuili Hospital · CNSecond Affiliated Hospital of Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAT-rich interactive domain-containing protein 1A (ARID1A) is a subunit of the mammary SWI/SNF chromatin remodeling complex and a tumor suppressor protein. The loss of ARID1A been observed in several types of human cancers and associated with poor patient prognosis. Previously, we have reported that ARID1A protein was rapidly ubiquitinated and destructed in gastric cancer cells during DNA damage response. However, the ubiquitin e3 ligase that mediated this process remains unclear. MATERIALS AND

methodsThe interaction between ARID1A and β-TRCP was verified by co-immunoprecipitation (Co-IP) assay. The degron site of ARID1A protein was analyzed by bioinformatics assay. Short hairpin RNAs (shRNAs) were used to knockdown (KD) gene expression.

resultsHere we show that DNA damage promotes ARID1A ubiquitination and subsequent destruction via the ubiquitin E3 ligase complex SCFβ-TRCP. β-TRCP recognizes ARID1A through a canonical degron site (DSGXXS) after its phosphorylation in response to DNA damage. Notably, genetic inactivation of the Ataxia Telangiectasia Mutated (ATM) kinase impaired DNA damage-induced ARID1A destruction.

conclusionsOur studies provide a novel molecular mechanism for the negative regulation of ARID1A by β-TRCP and ATM in DNA damaged gastric cancer cells.

Indexed as

ARID1ADNA damagePhosphodegronβ-TRCP

Identifiers

PMID31210753
PMCPMC6567580
OpenAlexW2950601245

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.