ArticleThe EMBO journal2010
IBRDC2, an IBR-type E3 ubiquitin ligase, is a regulatory factor for Bax and apoptosis activation.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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Who cites it
58 citing papers in PubMed, 89 citations in OpenAlex.
- Ubiquitin-Specific Protease 49 Interacts with Bax to Modulate Apoptosis.International journal of molecular sciences · 2026Article
- Targeted Mitochondrial ECSIT Overexpression Attenuates MASH by Increasing OTUD3 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TOM20-driven E3 ligase recruitment regulates mitochondrial dynamics through PLD6.Nature chemical biology · 2026Article
- E3 ubiquitin ligase NKLAM/RNF19b suppresses myc-driven B cell lymphomagenesis in Eμ-myc mice.Frontiers in oncology · 2026Article
- Ubiquitin-mediated degradation restricts spatiotemporal accumulation of the cytoplasmic male sterility protein WA352 to anthers in rice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cul5bioRxiv : the preprint server for biology · 2025Article
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- Genome-wide association study in chondrocalcinosis reveals ENPP1 as a candidate therapeutic target in calcium pyrophosphate deposition disease.Annals of the rheumatic diseases · 2025Article
- Apoptosis signaling is activated as a transient pulse in neurons.Cell death and differentiation · 2025Article
- Post-Translational Modifications of Proteins Orchestrate All Hallmarks of Cancer.Life (Basel, Switzerland) · 2025Review
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth.EMBO reports · 2024Article
- RNF144B negatively regulates antiviral immunity by targeting MDA5 for autophagic degradation.EMBO reports · 2024Article
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024Article
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle ImplicatesbioRxiv : the preprint server for biology · 2024Article
- Ubiquitin-proteasome pathway-mediated regulation of the Bcl-2 family: effects and therapeutic approaches.Haematologica · 2024Review
- Deubiquitinases in cancer.Nature reviews. Cancer · 2023Review
- The E3 ubiquitin ligase TRIM17 promotes gastric cancer survival and progression via controlling BAX stability and antagonizing apoptosis.Cell death and differentiation · 2023Article
- Rnf144b alleviates the inflammatory responses and cardiac dysfunction in sepsis.ESC heart failure · 2023Article
- Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Bax, a pro-apoptotic protein from the Bcl-2 family, is central to apoptosis regulation. To suppress spontaneous apoptosis, Bax must be under stringent control that may include regulation of Bax conformation and expression levels. We report that IBRDC2, an IBR-type RING-finger E3 ubiquitin ligase, regulates the levels of Bax and protects cells from unprompted Bax activation and cell death. Downregulation of IBRDC2 induces increased cellular levels and accumulation of the active form of Bax. The ubiquitination-dependent regulation of Bax stability is suppressed by IBRDC2 downregulation and stimulated by IBRDC2 overexpression in both healthy and apoptotic cells. Although mostly cytosolic in healthy cells, upon induction of apoptosis, IBRDC2 accumulates in mitochondrial domains enriched with Bax. Mitochondrial accumulation of IBRDC2 occurs in parallel with Bax activation and also depends on the expression levels of Bcl-xL. Furthermore, IBRDC2 physically interacts with activated Bax. By applying Bax mutants in HCT116 Bax(-/-) cells, combined with the use of active Bax-specific antibodies, we have established that both mitochondrial localization and apoptotic activation of Bax are required for IBRDC2 translocation to the mitochondria.
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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.