ArticleEMBO reports2019
Regulation of MAGE-A3/6 by the CRL4-DCAF12 ubiquitin ligase and nutrient availability.
Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Cysteine availability tunes ubiquitin signaling via inverse stability of LRRC58 E3 ligase and its substrate CDO1.Nature communications · 2026Article
- Article
- DCAF12 Ubiquitin Ligase Promotes Lung Cancer Metastasis by Modulating the TRiC/CCT Chaperonin Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Degrons: defining the rules of protein degradation.Nature reviews. Molecular cell biology · 2025Review
- S100A9 enhances tumor immune suppression and cancer cell survival in small cell lung cancer.Cell death & disease · 2025Article
- CRL4Nature communications · 2025Article
- Review
- Review
- Short-term starvation inhibits CD36 N-glycosylation and downregulates USP7 UFMylation to alleviate RBPJ-maintained T cell exhaustion in liver cancer.Theranostics · 2025Article
- Ubiquitination regulates autophagy in cancer: simple modifications, promising targets.Journal of translational medicine · 2024Review
- Probing the CRL4PNAS nexus · 2024Article
- DUB3 is a MAGEA3 deubiquitinase and a potential therapeutic target in hepatocellular carcinoma.iScience · 2024Article
- Optical Control of Proteasomal Protein Degradation with a Photoswitchable Lipopeptide.Angewandte Chemie (International ed. in English) · 2024Article
- ELM-the Eukaryotic Linear Motif resource-2024 update.Nucleic acids research · 2024Article
- The Price of Human Evolution: Cancer-Testis Antigens, the Decline in Male Fertility and the Increase in Cancer.International journal of molecular sciences · 2023Review
- Ubiquitin-independent proteasomal degradation driven by C-degron pathways.Molecular cell · 2023Article
- Cancer testis antigen subfamilies: Attractive targets for therapeutic vaccine (Review).International journal of oncology · 2023Review
- Protamine 1 as a secreted colorectal cancer-specific antigen facilitating G1/S phase transition under nutrient stress conditions.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Recognition of the CCT5 di-Glu degron by CRL4The EMBO journal · 2023Article
- A theoretical framework of immune cell phenotypic classification and discovery.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Melanoma antigen genes (MAGEs) are emerging as important oncogenic drivers that are normally restricted to expression in male germ cells but are aberrantly expressed in cancers and promote tumorigenesis. Mechanistically, MAGEs function as substrate specifying subunits of E3 ubiquitin ligases. Thus, the activation of germline-specific genes in cancer can drive metabolic and signaling pathways through altered ubiquitination to promote tumorigenesis. However, the mechanisms regulating MAGE expression and activity are unclear. Here, we describe how the MAGE-A3/6 proteins that function as repressors of autophagy are downregulated in response to nutrient deprivation. Short-term cellular starvation promotes rapid MAGE-A3/6 degradation in a proteasome-dependent manner. Proteomic analysis reveals that degradation of MAGE-A3/6 is controlled by the CRL4-DCAF12 E3 ubiquitin ligase. Importantly, the degradation of MAGE-A3/6 by CRL4-DCAF12 is required for starvation-induced autophagy. These findings suggest that oncogenic MAGEs can be dynamically controlled in response to stress to allow cellular adaptation, autophagy regulation, and tumor growth and that CRL4-DCAF12 activity is responsive to nutrient status.
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Registered trials
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.