ArticleAutophagy2017
PTK2-mediated degradation of ATG3 impedes cancer cells susceptible to DNA damage treatment.
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Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
What it found
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- Histone deacetylase 6 deacetylates and ubiquitinates ATG3 to regulate autophagy.Cell death and differentiation · 2026Article
- Autophagy- and oxidative stress-related protein deregulation mediated by extracellular vesicles of human MJD/SCA3 iPSC-derived neuroepithelial stem cells and differentiated neural cultures.Cell death & disease · 2025Article
- Targeting secretory autophagy in solid cancers: mechanisms, immune regulation and clinical insights.Experimental hematology & oncology · 2025Review
- Japanese Flounder pol-miR-155 Is Involved inGenes · 2023Article
- Degradation Mechanism of Autophagy-Related Proteins and Research Progress.International journal of molecular sciences · 2022Review
- Binding Features and Functions of ATG3.Frontiers in cell and developmental biology · 2021Review
- miR-651-3p Enhances the Sensitivity of Hepatocellular Carcinoma to Cisplatin via Targeting ATG3-Mediated Cell Autophagy.Journal of oncology · 2021Article
- The DNA-damage response and nuclear events as regulators of nonapoptotic forms of cell death.Oncogene · 2020Review
- Review
- Suppression of Cardiac Autophagy by Hyperinsulinemia in Insulin Receptor-Deficient Hearts Is Mediated by Insulin-Like Growth Factor Receptor Signaling.Antioxidants & redox signaling · 2019Article
- ATG3, a Target of miR-431-5p, Promotes Proliferation and Invasion of Colon Cancer via Promoting Autophagy.Cancer management and research · 2019Article
- The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism.Cell death discovery · 2018Article
- Sensitization of tamoxifen-resistant breast cancer cells by Z-ligustilide through inhibiting autophagy and accumulating DNA damages.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Ke Maa Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Wan Fua Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Ming Tanga Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Chaohua Zhanga Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Tianyun Houa Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Ran Lia Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Xiaopeng Lua Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Yanan Wanga Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Jingyi Zhoua Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Xue Lia Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Luyao Zhanga Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Lina Wanga Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Ying Zhaoa Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Wei-Guo Zhua Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Peking University Health Science Center , Beijing , China.
Peking University · CNState Key Laboratory of Natural and Biomimetic Drugs
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATG3 (autophagy-related 3) is an E2-like enzyme essential for autophagy; however, it is unknown whether it has an autophagy-independent function. Here, we report that ATG3 is a relatively stable protein in unstressed cells, but it is degraded in response to DNA-damaging agents such as etoposide or cisplatin. With mass spectrometry and a mutagenesis assay, phosphorylation of tyrosine 203 of ATG3 was identified to be a critical modification for its degradation, which was further confirmed by manipulating ATG3
Indexed as
DNA DamageProteolysisAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsAutophagy-Related ProteinsCell Line, TumorCell ProliferationEtoposideFocal Adhesion Kinase 1MiceMice, KnockoutMitosisNeoplasmsPhosphorylationUbiquitin-Conjugating EnzymesAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsATG3 protein, humanAutophagy-Related ProteinsBAG3 protein, humanEtoposideFocal Adhesion Kinase 1PTK2 protein, humanUbiquitin-Conjugating EnzymesATG3cancer therapymitotic catastrophePTK2tyrosine phosphorylation
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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.