ArticleMolecular and cellular biochemistry2011
Deletion mutational analysis of BMRP, a pro-apoptotic protein that binds to Bcl-2.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Comprehensive Analysis of Immune-Related Mitochondrial Genes in Ischemic Stroke Through Integrated Bioinformatics and Validation.Biomedicines · 2026Article
- Genetic and epigenetic correlation between diabetic retinopathy and polycystic ovarian syndrome: in-silico analyses-experimental research.Annals of medicine and surgery (2012) · 2025Article
- An early Transcriptomic Investigation in Adult Patients with Spinal Muscular Atrophy Under Treatment with Nusinersen.Journal of molecular neuroscience : MN · 2024Article
- DAP3-mediated cell cycle regulation and its association with radioresistance in human lung adenocarcinoma cell lines.Journal of radiation research · 2023Article
- Abnormal Expression of Mitochondrial Ribosomal Proteins and Their Encoding Genes with Cell Apoptosis and Diseases.International journal of molecular sciences · 2020Review
- Mitochondrial ribosomes in cancer.Seminars in cancer biology · 2017Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Bcl-2 is an anti-apoptotic member of the Bcl-2 family of proteins that protects cells from apoptosis induced by a large variety of stimuli. The protein BMRP (MRPL41) was identified as a Bcl-2 binding partner and shown to have pro-apoptotic activity. We have performed deletion mutational analyses to identify the domain(s) of Bcl-2 and BMRP that are involved in the Bcl-2/BMRP interaction, and the region(s) of BMRP that mediate its pro-apoptotic activity. The results of these studies indicate that both the BH4 domain of Bcl-2 and its central region encompassing its BH1, BH2, and BH3 domains are required for its interaction with BMRP. The loop region and the transmembrane domain of Bcl-2 were found to be dispensable for this interaction. The Bcl-2 deletion mutants that do not interact with BMRP were previously shown to be functionally inactive. Deletion analyses of the BMRP protein delimited the region of BMRP needed for its interaction with Bcl-2 to the amino-terminal two-thirds of the protein (amino acid residues 1-92). Further deletions at either end of the BMRP(1-92) truncated protein resulted in lack of binding to Bcl-2. Functional studies performed with BMRP deletion mutants suggest that the cell death-inducing domains of the protein reside mainly within its amino-terminal two-thirds. The region of BMRP required for the interaction with Bcl-2 is very relevant for the cell death-inducing activity of the protein, suggesting that one possible mechanism by which BMRP induces cell death is by binding to and blocking the anti-apoptotic activity of Bcl-2.
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