ArticleThe Journal of biological chemistry2010
Facilitation of mitochondrial outer and inner membrane permeabilization and cell death in oxidative stress by a novel Bcl-2 homology 3 domain protein.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Article
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- C/EBPβ Regulates TFAM Expression, Mitochondrial Function and Autophagy in Cellular Models of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Use of gene expression profile to identify potentially relevant transcripts to myofibrillar fragmentation index trait.Functional & integrative genomics · 2020Article
- Unraveling Targetable Systemic and Cell-Type-Specific Molecular Phenotypes of Alzheimer's and Parkinson's Brains With Digital Cytometry.Frontiers in neuroscience · 2020Article
- Positive allosteric modulation of P2X7 promotes apoptotic cell death over lytic cell death responses in macrophages.Cell death & disease · 2019Article
- Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity.eLife · 2019Article
- Thermodynamic Characterization of the CaInternational journal of molecular sciences · 2018Article
- Liver Transcriptome and miRNA Analysis of Silver Carp (Frontiers in physiology · 2018Article
- Structural and Functional Study of Apoptosis-linked Gene-2·Heme-binding Protein 2 Interactions in HIV-1 Production.The Journal of biological chemistry · 2016Article
- Evolution of the SOUL Heme-Binding Protein Superfamily Across Eukarya.Journal of molecular evolution · 2016Article
- Role of mitochondrial network stabilisation by a human small heat shock protein in tumour malignancy.Journal of Cancer · 2015Article
- Plasminogen activator inhibitor 1, fibroblast apoptosis resistance, and aging-related susceptibility to lung fibrosis.Experimental gerontology · 2015Article
- An Integrated Bioinformatics and Computational Biology Approach Identifies New BH3-Only Protein Candidates.The open biology journal · 2012Article
- Possible predictors of histopathological response to neoadjuvant chemoradiotherapy for rectal cancer.Journal of cancer research and clinical oncology · 2012Article
- The inhibition of autophagy sensitises colon cancer cells with wild-type p53 but not mutant p53 to topotecan treatment.PloS one · 2012Article
- Carnosic acid, a rosemary phenolic compound, induces apoptosis through reactive oxygen species-mediated p38 activation in human neuroblastoma IMR-32 cells.Neurochemical research · 2011Article
- Structural changes in the BH3 domain of SOUL protein upon interaction with the anti-apoptotic protein Bcl-xL.The Biochemical journal · 2011Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We identified a sequence homologous to the Bcl-2 homology 3 (BH3) domain of Bcl-2 proteins in SOUL. Tissues expressed the protein to different extents. It was predominantly located in the cytoplasm, although a fraction of SOUL was associated with the mitochondria that increased upon oxidative stress. Recombinant SOUL protein facilitated mitochondrial permeability transition and collapse of mitochondrial membrane potential (MMP) and facilitated the release of proapoptotic mitochondrial intermembrane proteins (PMIP) at low calcium and phosphate concentrations in a cyclosporine A-dependent manner in vitro in isolated mitochondria. Suppression of endogenous SOUL by diced small interfering RNA in HeLa cells increased their viability in oxidative stress. Overexpression of SOUL in NIH3T3 cells promoted hydrogen peroxide-induced cell death and stimulated the release of PMIP but did not enhance caspase-3 activation. Despite the release of PMIP, SOUL facilitated predominantly necrotic cell death, as revealed by annexin V and propidium iodide staining. This necrotic death could be the result of SOUL-facilitated collapse of MMP demonstrated by JC-1 fluorescence. Deletion of the putative BH3 domain sequence prevented all of these effects of SOUL. Suppression of cyclophilin D prevented these effects too, indicating that SOUL facilitated mitochondrial permeability transition in vivo. Overexpression of Bcl-2 and Bcl-x(L), which can counteract the mitochondria-permeabilizing effect of BH3 domain proteins, also prevented SOUL-facilitated collapse of MMP and cell death. These data indicate that SOUL can be a novel member of the BH3 domain-only proteins that cannot induce cell death alone but can facilitate both outer and inner mitochondrial membrane permeabilization and predominantly necrotic cell death in oxidative stress.
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