ArticleArchives of biochemistry and biophysics2014
MAGE proteins regulate KRAB zinc finger transcription factors and KAP1 E3 ligase activity.
Article in Archives of biochemistry and biophysics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Comprehensively exploring the roles of MAGEA1 in cryptorchidism and its related transcription factor regulatory network.Journal of molecular histology · 2026Article
- TRIM28 in cancer and cancer therapy.Frontiers in genetics · 2024Review
- Expression of MAGE A1 to MAGE A10 in the Forceps Biopsy and Bronchoalveolar Lavage Specimens from Patients with the Central Lung Tumor.Asian Pacific journal of cancer prevention : APJCP · 2024Observational
- Cancer testis antigen subfamilies: Attractive targets for therapeutic vaccine (Review).International journal of oncology · 2023Review
- Generation of TRIM28 Knockout K562 Cells by CRISPR/Cas9 Genome Editing and Characterization of TRIM28-Regulated Gene Expression in Cell Proliferation and Hemoglobin Beta Subunits.International journal of molecular sciences · 2022Article
- Transcriptomic characterization of cancer-testis antigens identifies MAGEA3 as a driver of tumor progression in hepatocellular carcinoma.PLoS genetics · 2021Article
- Emerging roles of the MAGE protein family in stress response pathways.The Journal of biological chemistry · 2020Review
- Functional and mechanistic studies reveal MAGEA3 as a pro-survival factor in pancreatic cancer cells.Journal of experimental & clinical cancer research : CR · 2019Article
- Tumor suppressive miR-6775-3p inhibits ESCC progression through forming a positive feedback loop with p53 via MAGE-A family proteins.Cell death & disease · 2018Article
- Cellular and disease functions of the Prader-Willi Syndrome geneThe Biochemical journal · 2017Review
- A Comprehensive Guide to the MAGE Family of Ubiquitin Ligases.Journal of molecular biology · 2017Review
- ZNF224, Krüppel like zinc finger protein, induces cell growth and apoptosis-resistance by down-regulation of p21 and p53 via miR-663a.Oncotarget · 2016Article
- Structures of Two Melanoma-Associated Antigens Suggest Allosteric Regulation of Effector Binding.PloS one · 2016Article
- The MAGE protein family and cancer.Current opinion in cell biology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Expression of Melanoma AntiGen Encoding (MAGE) genes, particularly MAGE-A3, has been correlated with aggressive clinical course, the acquisition of resistance to chemotherapy and poor clinical outcomes of melanoma and other malignancies. MAGE proteins bind to KAP1, a gene repressor and ubiquitin E3 ligase which also binds KRAB domain containing zinc finger transcription factors (KZNFs), and MAGE expression may affect KZNF mediated gene regulation. To investigate mechanisms for these effects, we tested the hypothesis that differences in KRAB domain composition affect KZNF poly-ubiquitination and determine whether MAGE expression increases, decreases, or has no effect on KZNFs mediated gene repression. Using an integrated reporter gene responsive to repression by KRAB domain fusion proteins, we found that MAGE-A3 relieved KZNF mediated repression and induced KZNF poly-ubiquitination and degradation in association with expression of the A+B box KRAB domain. In contrast, MAGE-A3 enhanced KAP1 mediated repression of KZNFs expressing A or A+b box KRAB domains but caused no increase in poly-ubiquitination or degradation. MAGE-A3 has no significant impact on KZNFs with KRAB domains containing the Scan box motif. These data support our hypothesis by showing that the effects of MAGE-A3 on gene repression depend on the type of KZNF KRAB domain involved.
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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.