The MAGE protein family and cancer
Open accessAbstract
The Melanoma Antigen Gene (MAGE) protein family is a large, highly conserved group of proteins that share a common MAGE homology domain. Intriguingly, many MAGE proteins are restricted in expression to reproductive tissues, but are aberrantly expressed in a wide variety of cancer types. Originally discovered as antigens on tumor cells and developed as cancer immunotherapy targets, recent literature suggests a more prominent role for MAGEs in driving tumorigenesis. This review will highlight recent developments into the function of MAGEs as oncogenes, their mechanisms of action in regulation of ubiquitin ligases, and outstanding questions in the field.
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The MAGE family of ubiquitin E3 ligases, often called MAGE-RING ligases (MRLs), comprise proteins that serve as substrate-recruitment modules for other RING E3 ligases, adding to and/or altering the substrate specificity of their co-E3 ligases.
“An example of such a family of ligases are the MAGE (melanoma antigen genes) family of ubiquitin E3 ligases, often referred to as the MAGE-RING ligases (MRLs), which comprise proteins that serve as substrate-recruitment modules for other RING E3 ligases156,157, adding to and/or altering the substrate specificity of their co-E3 ligases (reviewed elsewhere155,158).”
From PROTAC targeted protein degraders: the past is prologue (2022) · cites this paper as [155]
Cancer-testis antigens comprise ubiquitin ligases that have restricted expression in normal testis but are highly overexpressed across multiple cancer types.
“Finally, cancer-testis antigens (CTAs) also comprise ubiquitin ligases that have restricted expression in the normal testis but are highly overexpressed across multiple cancer types154,155.”
From PROTAC targeted protein degraders: the past is prologue (2022) · cites this paper as [155]
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- Authors
- Weon, J. L., & Potts, P. R.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Potts, Patrick Ryan
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2015-12
- Volume
- 37
- Pages
- 1-8
- ISSN
- 0955-0674 (ISSN-L)
- PMC
- PMC4688208
- OpenAlex
- W1254044211
- Cited by
- 257
- References
- 80
- Citations by year
- 2026: 14 · 2025: 18 · 2024: 40 · 2023: 28 · 2022: 31 · 2021: 30 · 2020: 36 · 2019: 15 · 2018: 23 · 2017: 15 · 2016: 7
- FWCI
- 1.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Current Opinion in Cell Biology (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense (W81XWH-12-1-0446)
- National Institutes of Health (R01GM111332)
- American Cancer Society (IRG 02-196)
- Cancer Prevention and Research Institute of Texas (R1117)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- oncogenes, carcinogenesis, cancer immunotherapy targets, ubiquitin ligase
- MeSH terms
- Animals, Antigens, Neoplasm, Humans, Immunotherapy, Neoplasm Proteins, Neoplasms, Neoplastic Stem Cells, Disease Progression
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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