ArticleMolecular biology of the cell2016
Mitochondrial E3 ubiquitin ligase MARCH5 controls mitochondrial fission and cell sensitivity to stress-induced apoptosis through regulation of MiD49 protein.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.
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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
97 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Roles of mitochondrial fusion and fission in breast cancer progression: a systematic review.World journal of surgical oncology · 2022Pooled it
- Cell-Type-Specific Calibration of Mitochondrial Ubiquitination in Stem Cell Fate Decisions.Stem cell reviews and reports · 2026Review
- Review
- Mechanisms of Action of FUNDC1 in Cerebral Ischemia-Reperfusion Injury.Molecular neurobiology · 2026Review
- Mitochondrial dynamics and cancer: mechanisms and targeted therapy.Cell biology and toxicology · 2026Review
- Regulation of mitochondrial biogenesis and energy metabolism in the heart.Chinese medical journal · 2026Review
- What does BCL-2 do? From new molecular insights to the clinical implications.Cell death and differentiation · 2026Review
- Neuronal mitochondrial dynamics: roles in brain disorders and therapeutic potential.Acta pharmacologica Sinica · 2026Article
- MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026Article
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- The many faces of p97/Cdc48 in mitochondrial homeostasis.Essays in biochemistry · 2025Review
- Review
- Review
- Mitochondrial proteome landscape unveils key insights into melanoma severity and treatment strategies.Cancer · 2025Article
- The E3 ubiquitin ligase MARCH5 promotes mitochondrial fusion and cell-cycle progression in acute myeloid leukemia.Blood advances · 2025Article
- Outer mitochondrial membrane E3 Ub ligase MARCH5 controls de novo peroxisome biogenesis.Developmental cell · 2025Article
- Inhibiting MARCH5/Mfn2 signaling as an alternative strategy to protect cardiomyocytes from hypoxia-induced mitochondrial dysfunction.Computational and structural biotechnology journal · 2025Article
- Exploring mitochondrial dynamics and localization under cellular stress: A comprehensive insight.Journal of biosciences · 2025Review
- Ubiquitination regulation of mitochondrial homeostasis: a new sight for the treatment of gastrointestinal tumors.Frontiers in immunology · 2025Review
- Deciphering MARCH5's impact on multiple myeloma: insights into autophagy regulation and AKT-FOXO3 signaling.Blood neoplasia · 2024Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Ubiquitin- and proteasome-dependent outer mitochondrial membrane (OMM)-associated degradation (OMMAD) is critical for mitochondrial and cellular homeostasis. However, the scope and molecular mechanisms of the OMMAD pathways are still not well understood. We report that the OMM-associated E3 ubiquitin ligase MARCH5 controls dynamin-related protein 1 (Drp1)-dependent mitochondrial fission and cell sensitivity to stress-induced apoptosis. MARCH5 knockout selectively inhibited ubiquitination and proteasomal degradation of MiD49, a mitochondrial receptor of Drp1, and consequently led to mitochondrial fragmentation. Mitochondrial fragmentation in MARCH5(-/-) cells was not associated with inhibition of mitochondrial fusion or bioenergetic defects, supporting the possibility that MARCH5 is a negative regulator of mitochondrial fission. Both MARCH5 re-expression and MiD49 knockout in MARCH5(-/-) cells reversed mitochondrial fragmentation and reduced sensitivity to stress-induced apoptosis. These findings and data showing MARCH5-dependent degradation of MiD49 upon stress support the possibility that MARCH5 regulation of MiD49 is a novel mechanism controlling mitochondrial fission and, consequently, the cellular response to stress.
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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.