ArticleCell death and differentiation2019
TRIM17 and TRIM28 antagonistically regulate the ubiquitination and anti-apoptotic activity of BCL2A1.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 68 citations in OpenAlex.
- TRIM17 downregulation modulates CRPC progression and enzalutamide resistance by derepressing BCL2 expression via the p53-dependent and p53-independent pathways.Cell death and differentiation · 2026Article
- Anti-apoptotic BCL-2 family proteins: from regulatory networks to therapeutic targeting.Oncogenesis · 2026Review
- Inhibition of RNA polymerase II-activating CDK9 and CDK12/13, but not of cell cycle relevant CDKs, induces apoptosis by downregulating the short-lived Bcl-2 proteins Mcl1 and Bfl1/A1.Cell death & disease · 2026Article
- TIF1 Family Proteins as Modulators of Cell Death: Mechanisms and Therapeutic Opportunities.Biomolecules · 2026Review
- RING finger E3 ubiquitin ligases: novel therapeutic opportunities in melanoma.Cellular & molecular biology letters · 2026Review
- PMM2 interacts with TRIM28 to recruit E2F4 and promote KIFC3-mediated tumor glycolysis and colorectal cancer progression.Oncogene · 2026Article
- TRIM28 contributes to epidermal homeostasis and is associated with altered p53 regulation.Frontiers in cell and developmental biology · 2026Article
- TRIM63/IRF-8 axis promotes tumor progression and immunosuppression of melanoma with BRAF mutation.Cell death & disease · 2025Article
- TRIM17 promotes the progression of osteosarcoma by regulating PDK1 m6A modification-mediated AKT/mTOR pathway activation through ubiquitination of FTO.Cell death & disease · 2025Article
- Reciprocal stabilization of CtBP and TRIM28 represses autophagy to promote metastasis.Nature structural & molecular biology · 2025Article
- March5-mediated Trim28 degradation preserves islet β-cell function in mice.Nature communications · 2025Article
- ZSCAN21 mediates the pathogenic transcriptional induction of α-synuclein in cellular and animal models of Parkinson's disease.Cell death & disease · 2025Article
- Multifaceted role ofMedComm · 2024Review
- Contribution of A1 to macrophage survival in cooperation with MCL-1 and BCL-XCell death & disease · 2024Article
- Satellite cell-derived TRIM28 is pivotal for mechanical load- and injury-induced myogenesis.EMBO reports · 2024Article
- Decreased GATA3 levels cause changed mouse cutaneous innate lymphoid cell fate, facilitating hair follicle recycling.Developmental cell · 2024Article
- Review
- KAP1 stabilizes MYCN mRNA and promotes neuroblastoma tumorigenicity by protecting the RNA mJournal of experimental & clinical cancer research : CR · 2024Article
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
- TRIM28 in cancer and cancer therapy.Frontiers in genetics · 2024Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BCL2A1 is an anti-apoptotic member of the BCL-2 family that contributes to chemoresistance in a subset of tumors. BCL2A1 has a short half-life due to its constitutive processing by the ubiquitin-proteasome system. This constitutes a major tumor-suppressor mechanism regulating BCL2A1 function. However, the enzymes involved in the regulation of BCL2A1 protein stability are currently unknown. Here, we provide the first insight into the regulation of BCL2A1 ubiquitination. We present evidence that TRIM28 is an E3 ubiquitin-ligase for BCL2A1. Indeed, endogenous TRIM28 and BCL2A1 bind to each other at the mitochondria and TRIM28 knock-down decreases BCL2A1 ubiquitination. We also show that TRIM17 stabilizes BCL2A1 by blocking TRIM28 from binding and ubiquitinating BCL2A1, and that GSK3 is involved in the phosphorylation-mediated inhibition of BCL2A1 degradation. BCL2A1 and its close relative MCL1 are thus regulated by common factors but with opposite outcome. Finally, overexpression of TRIM28 or knock-out of TRIM17 reduced BCLA1 protein levels and restored sensitivity of melanoma cells to BRAF-targeted therapy. Therefore, our data describe a molecular rheostat in which two proteins of the TRIM family antagonistically regulate BCL2A1 stability and modulate cell death.
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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.