ArticleCell death and differentiation2023
MARCH5 regulates mitotic apoptosis through MCL1-dependent and independent mechanisms.
Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Cell-Type-Specific Calibration of Mitochondrial Ubiquitination in Stem Cell Fate Decisions.Stem cell reviews and reports · 2026Review
- The mitochondrial ubiquitin ligase MARCHF5 cooperates with MCL1 to inhibit apoptosis in KSHV-transformed primary effusion lymphoma cell lines.PLoS pathogens · 2026Article
- GET3 regulates apoptosis via tail-anchoring of MCL1.Cell death and differentiation · 2026Article
- Elucidating molecularly stratified single agent, and combination, therapeutic strategies targeting MCL1 for lethal prostate cancer.Nature communications · 2025Article
- The roles of ubiquitination in AML.Annals of hematology · 2024Review
- Pan-cancer evaluation of regulated cell death to predict overall survival and immune checkpoint inhibitor response.NPJ precision oncology · 2024Article
- BCL-XL regulates the timing of mitotic apoptosis independently of BCL2 and MCL1 compensation.Cell death & disease · 2024Article
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-apoptotic MCL1 is critical for delaying apoptosis during mitotic arrest. MCL1 is degraded progressively during mitotic arrest, removing its anti-apoptotic function. We found that knockout of components of ubiquitin ligases including APC/C, SCF complexes, and the mitochondrial ubiquitin ligase MARCH5 did not prevent mitotic degradation of MCL1. Nevertheless, MARCH5 determined the initial level of MCL1-NOXA network upon mitotic entry and hence the window of time during MCL1 was present during mitotic arrest. Paradoxically, although knockout of MARCH5 elevated mitotic MCL1, mitotic apoptosis was in fact enhanced in a BAK-dependent manner. Mitotic apoptosis was accelerated after MARCH5 was ablated in both the presence and absence of MCL1. Cell death was not altered after disrupting other MARCH5-regulated BCL2 family members including NOXA, BIM, and BID. Disruption of the mitochondrial fission factor DRP1, however, reduced mitotic apoptosis in MARCH5-disrupted cells. These data suggest that MARCH5 regulates mitotic apoptosis through MCL1-independent mechanisms including mitochondrial maintenance that can overcome the stabilization of MCL1.
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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.