ArticlePloS one2011
Identification of a conserved anti-apoptotic protein that modulates the mitochondrial apoptosis pathway.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
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- Panoramic analysis of cell death patterns reveals prognostic and immune profiles of head and neck squamous cell carcinoma.American journal of cancer research · 2024Article
- Single-cell characterization of step-wise acquisition of carboplatin resistance in ovarian cancer.NPJ systems biology and applications · 2022Article
- Genome-Wide Association Study of Metamizole-Induced Agranulocytosis in European Populations.Genes · 2020Article
- Article
- MKL1/miR-5100/CAAP1 loop regulates autophagy and apoptosis in gastric cancer cells.Neoplasia (New York, N.Y.) · 2020Article
- Towards an understanding of C9orf82 protein/CAAP1 function.PloS one · 2019Article
- Three-Dimensional Cellular Arrangement in Epithelial Ovarian Cancer Cell Lines TOV-21G and SKOV-3 is Associated with Apoptosis-Related miRNA Expression Modulation.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2018Article
- Topoisomerase II Poisons for Glioblastoma; Existing Challenges and Opportunities to Personalize Therapy.Frontiers in neurology · 2018Review
- Genetic rearrangements result in altered gene expression and novel fusion transcripts in Sézary syndrome.Oncotarget · 2017Article
- Differential Gene Expression Patterns in Chicken Cardiomyocytes during Hydrogen Peroxide-Induced Apoptosis.PloS one · 2016Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Here we identified an evolutionarily highly conserved and ubiquitously expressed protein (C9orf82) that shows structural similarities to the death effector domain of apoptosis-related proteins. RNAi knockdown of C9orf82 induced apoptosis in A-549 and MCF7/casp3-10b lung and breast carcinoma cells, respectively, but not in cells lacking caspase-3, caspase-10 or both. Apoptosis was associated with activated caspases-3, -8, -9 and -10, and inactivation of caspases 10 or 3 was sufficient to block apoptosis in this pathway. Apoptosis upon knockdown of C9orf82 was associated with increased caspase-10 expression and activation, which was required for the generation of an 11 kDa tBid fragment and activation of Caspase-9. These data suggest that C9orf82 functions as an anti-apoptotic protein that modulates a caspase-10 dependent mitochondrial caspase-3/9 feedback amplification loop. We designate this ubiquitously expressed and evolutionarily conserved anti-apoptotic protein Conserved Anti-Apoptotic Protein (CAAP). We also demonstrated that treatment of MCF7/casp3-10b cells with staurosporine and etoposides induced apoptosis and knockdown of CAAP expression. This implies that the CAAP protein could be a target for chemotherapeutic agents.
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Registered trials
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