ArticleOncogene2002
Activation of mitochondrial voltage-dependent anion channel by apro-apoptotic BH3-only protein Bim.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 120 citations in OpenAlex.
- VDAC1-interacting proteins: binding site mapping and their derived peptides induce apoptosis and multifaceted cellular effects.Apoptosis : an international journal on programmed cell death · 2025Article
- VDAC1-Based Peptides as Potential Modulators of VDAC1 Interactions with Its Partners and as a Therapeutic for Cancer, NASH, and Diabetes.Biomolecules · 2024Review
- VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases.Biomolecules · 2020Review
- Effects of ABT-737 combined with irradiation treatment on uterine cervical cancer cells.Oncology letters · 2019Article
- Ventilator-induced diaphragm dysfunction in critical illness.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Targeting Mitochondrial Ion Channels to Fight Cancer.International journal of molecular sciences · 2018Review
- Selective induction of cancer cell death by VDAC1-based peptides and their potential use in cancer therapy.Molecular oncology · 2018Article
- VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress.Cell stress · 2017Article
- Voltage-Dependent Anion Channel 1 As an Emerging Drug Target for Novel Anti-Cancer Therapeutics.Frontiers in oncology · 2017Review
- The Mitochondrial Voltage-Dependent Anion Channel 1, CaFrontiers in oncology · 2017Review
- Mitochondrial ATF2 translocation contributes to apoptosis induction and BRAF inhibitor resistance in melanoma through the interaction of Bim with VDAC1.Oncotarget · 2015Article
- Yeast as a tool for studying proteins of the Bcl-2 family.Microbial cell (Graz, Austria) · 2015Review
- Genes associated with sodium fluoride-induced human osteoblast apoptosis.International journal of clinical and experimental medicine · 2015Article
- Human Bop is a novel BH3-only member of the Bcl-2 protein family.Protein & cell · 2012Article
- NDV-induced apoptosis in absence of Bax; evidence of involvement of apoptotic proteins upstream of mitochondria.Virology journal · 2012Article
- VDAC1: from structure to cancer therapy.Frontiers in oncology · 2012Article
- Anti-tumour effects of xanthone derivatives and the possible mechanisms of action.Investigational new drugs · 2011Article
- Intrinsic apoptosis in mechanically ventilated human diaphragm: linkage to a novel Fos/FoxO1/Stat3-Bim axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Inhibition of Bak activation by VDAC2 is dependent on the Bak transmembrane anchor.The Journal of biological chemistry · 2010Article
- Mitochondria-centric activation induced cell death of cytolytic T lymphocytes and its implications for cancer immunotherapy.Vaccine · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bcl-2 family of proteins regulates apoptosis by controlling mitochondrial membrane permeability. We have previously shown that the voltage-dependent anion channel (VDAC) plays a crucial role in apoptotic changes of the mitochondria and its activity is directly regulated by some Bcl-2 family members, including Bcl-2/Bcl-x(L) and Bax/Bak but not Bid. Here, we showed that in isolated mitochondria, Bim induced loss of membrane potential and cytochrome c release like Bax/Bak, with these changes being inhibited by an anti-VDAC antibody. In addition, microinjection of the anti-VDAC antibody significantly reduced Bim-induced apoptosis. Study using purified proteins indicated that Bim directly interacts with the VDAC. Immunoprecipitation analysis revealed that Bim interacts with the VDAC and the interaction is remarkably enhanced during apoptosis. An experiment using liposomes indicated that Bim enhanced VDAC activity, as did Bax/Bak. Furthermore, Bim (but not tBid) was able to induce apoptotic changes of yeast mitochondria in a VDAC-dependent manner, and also induced the lysis of red blood cells, with this effect being inhibited by the anti-VDAC antibody. These results indicate that Bim has an ability to activate directly the VDAC, which plays an important role in apoptosis of mammalian cells.
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Registered trials
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.