ArticleGenes & cancer2013
BaxΔ2 Family Alternative Splicing Salvages Bax Microsatellite-Frameshift Mutations.
Article in Genes & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- A Darwinian Perspective on Tumor Evolution.International journal of biological sciences · 2026Review
- Alternative production of pro-death Bax∆2 protein via ribosomal frameshift in Alzheimer's disease.Scientific reports · 2024Article
- Unconventional Source of Neurotoxic Protein Aggregation from Organelle Off-Target Bax∆2 in Alzheimer's Disease.Biomolecules · 2023Article
- A Structural Model for Bax∆2-Mediated Activation of Caspase 8-Dependent Apoptosis.International journal of molecular sciences · 2020Article
- Immunohistochemical detection of the pro-apoptotic Bax∆2 protein in human tissues.Histochemistry and cell biology · 2020Article
- Nanopore label-free detection of single-nucleotide deletion in Baxα/BaxΔ2.Electrophoresis · 2018Article
- Detection of pro-apoptotic Bax∆2 proteins in the human cerebellum.Histochemistry and cell biology · 2018Article
- BaxΔ2 sensitizes colorectal cancer cells to proteasome inhibitor-induced cell death.Biochemical and biophysical research communications · 2018Article
- The functional domains for Bax∆2 aggregate-mediated caspase 8-dependent cell death.Experimental cell research · 2017Article
- BaxΔ2 promotes apoptosis through caspase-8 activation in microsatellite-unstable colon cancer.Molecular cancer research : MCR · 2014Article
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Authors and funding
7 authors.
Funding
Abstract
Mutation or aberrant splicing can interrupt gene expression. Tumor suppressor Bax is one of the susceptible genes prone to microsatellite frameshifting mutations in coding regions. As a result, tumors exhibiting microsatellite instability (MSI) often present a "Bax-negative" phenotype. We previously reported that some Bax-negative cells in fact contain a functional Bax isoform (BaxΔ2), generated when unique alternative splicing "salvages" the shifted reading frame introduced by a microsatellite mutation. Here we compared Bax alternative splicing profiles in a range of cell lines and primary tumors with and without Bax microsatellite mutations. We found that MSI tumors exhibit a high Bax alternative splicing frequency, especially in exon 2, and produce a family of alternatively spliced isoforms that retain many important Bax functional domains. Surprisingly, these BaxΔ2 family isoforms can rescue Bax from all common microsatellite frameshift mutations. Production of BaxΔ2 requires specific cis mutations, while trans components are not cell-type specific. Furthermore, all BaxΔ2 family isoforms are more potent cell death inducers than the parental Bax without directly targeting mitochondria. These results indicate that the BaxΔ2 family can potentially salvage Bax tumor suppressor expression otherwise lost to mutation.
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