ArticleMolecular and cellular biology2007
Methylation-controlled J protein promotes c-Jun degradation to prevent ABCB1 transporter expression.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
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Who cites it
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.
- Meta-analysis of gene signatures and key pathways indicates suppression of JNK pathway as a regulator of chemo-resistance in AML.Scientific reports · 2021Pooled it
- Hypermethylation of tumor suppressor genes is a risk factor for poor prognosis in ovarian cancer: A meta-analysis.Medicine · 2019Pooled it
- Review
- Modulation of the immunogenic landscape in colorectal cancer by mitochondrial methylation-controlled J protein.Molecular biomedicine · 2026Article
- Deleting the mitochondrial respiration negative regulator MCJ enhances the efficacy of CD8Nature communications · 2024Article
- The role of DNA methylation in ovarian cancer chemoresistance: A narrative review.Health science reports · 2023Article
- Chemotherapy and Physical Therapeutics Modulate Antigens on Cancer Cells.Frontiers in immunology · 2022Review
- Regulation of p53 and Cancer Signaling by Heat Shock Protein 40/J-Domain Protein Family Members.International journal of molecular sciences · 2021Review
- Boosting mitochondria activity by silencing MCJ overcomes cholestasis-induced liver injury.JHEP reports : innovation in hepatology · 2021Article
- Mitochondrial ATP fuels ABC transporter-mediated drug efflux in cancer chemoresistance.Nature communications · 2021Article
- Silencing hepatic MCJ attenuates non-alcoholic fatty liver disease (NAFLD) by increasing mitochondrial fatty acid oxidation.Nature communications · 2020Article
- Role of Mycoplasma Chaperone DnaK in Cellular Transformation.International journal of molecular sciences · 2020Review
- Glycolysis Induces MCJ Expression That Links T Cell Proliferation With Caspase-3 Activity and Death.Frontiers in cell and developmental biology · 2019Article
- ETV7-Mediated DNAJC15 Repression Leads to Doxorubicin Resistance in Breast Cancer Cells.Neoplasia (New York, N.Y.) · 2018Article
- Functional Diversity of Human Mitochondrial J-proteins Is Independent of Their Association with the Inner Membrane Presequence Translocase.The Journal of biological chemistry · 2016Article
- Integration and bioinformatics analysis of DNA-methylated genes associated with drug resistance in ovarian cancer.Oncology letters · 2016Article
- Fine-Tuning of CD8(+) T Cell Mitochondrial Metabolism by the Respiratory Chain Repressor MCJ Dictates Protection to Influenza Virus.Immunity · 2016Article
- Deficiency of mitochondrial modulator MCJ promotes chemoresistance in breast cancer.JCI insight · 2016Article
- Ikaros mediates the DNA methylation-independent silencing of MCJ/DNAJC15 gene expression in macrophages.Scientific reports · 2015Article
- Rewired metabolism in drug-resistant leukemia cells: a metabolic switch hallmarked by reduced dependence on exogenous glutamine.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylation-controlled J protein (MCJ) is a newly identified member of the DnaJ family of cochaperones. Hypermethylation-mediated transcriptional silencing of the MCJ gene has been associated with increased chemotherapeutic resistance in ovarian cancer. However, the biology and function of MCJ remain unknown. Here we show that MCJ is a type II transmembrane cochaperone localized in the Golgi network and present only in vertebrates. MCJ is expressed in drug-sensitive breast cancer cells but not in multidrug-resistant cells. The inhibition of MCJ expression increases resistance to specific drugs by inducing expression of the ABCB1 drug transporter that prevents intracellular drug accumulation. The induction of ABCB1 gene expression is mediated by increased levels of c-Jun due to an impaired degradation of this transcription factor in the absence of MCJ. Thus, MCJ is required in these cells to prevent c-Jun-mediated expression of ABCB1 and maintain drug response.
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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.