ArticleThe Journal of biological chemistry2013
An interaction between Bcl-xL and the voltage-dependent anion channel (VDAC) promotes mitochondrial Ca2+ uptake.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Intermembrane coupling between Bcl-xL and the IPCell reports · 2026Article
- Mitochondrial Voltage-Dependent Anion Channel: From a Passive Pore to a Cellular Hub Through Protein Complexation.International journal of molecular sciences · 2026Review
- Survivin Associates with VDAC2 and Bcl2-Family Proteins at the Mitochondrial Outer Membrane.International journal of molecular sciences · 2026Article
- A pore is a pore is a pore (or a hub?): VDAC oligomerization in mitochondrial connectivity and modulation.Biochemical Society transactions · 2026Review
- VDAC1: The mitochondrial gatekeeper in the battle against hearing loss (Review).Biomedical reports · 2025Review
- Structural basis of apoptosis induction by the mitochondrial voltage-dependent anion channel.Nature communications · 2025Article
- Cell death and cancer: Metabolic interconnections.Cell reports · 2025Review
- Bcl-2 and Bcl-xL in Diabetes: Contributions to Endocrine Pancreas Viability and Function.Biomedicines · 2025Review
- The role of mitochondria-associated ER membranes in disease pathology: protein complex and therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- VDAC1-Based Peptides as Potential Modulators of VDAC1 Interactions with Its Partners and as a Therapeutic for Cancer, NASH, and Diabetes.Biomolecules · 2024Review
- The endoplasmic reticulum pool of Bcl-xL prevents cell death through IP3R-dependent calcium release.Cell death discovery · 2024Article
- FGF4 protects the liver from immune-mediated injury by activating CaMKKActa pharmaceutica Sinica. B · 2024Article
- Single-cell RNA sequencing reveals Immune Education promotes T cell survival in mice subjected to the cecal ligation and puncture sepsis model.Frontiers in immunology · 2024Article
- Voltage-dependent anion channel 1 (VDAC1) overexpression alleviates cardiac fibroblast activation in cardiac fibrosis via regulating fatty acid metabolism.Redox biology · 2023Article
- Ratiometric measurement of MAM CaNature communications · 2023Article
- [High expression of MYH9 inhibits apoptosis of non-small cell lung cancer cells through activating the AKT/c-Myc pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Voltage-Dependent Anion Channel 1 Expression in Oral Malignant and Premalignant Lesions.Diagnostics (Basel, Switzerland) · 2023Article
- 4-Phenylbutyrate Mitigates the Motor Impairment and Dopaminergic Neuronal Death During Parkinson's Disease Pathology via Targeting VDAC1 Mediated Mitochondrial Function and Astrocytes Activation.Neurochemical research · 2022Article
- Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The role of the antiapoptotic protein Bcl-xL in regulating mitochondrial Ca(2+) ([Ca(2+)]mito) handling was examined in wild-type (WT) and Bcl-xL knock-out (Bcl-xL-KO) mouse embryonic fibroblast cells. Inositol 1,4,5-trisphosphate-generating agonist evoked cytosolic Ca(2+) transients that produced a larger [Ca(2+)]mito uptake in WT cells compared with Bcl-xL-KO. In permeabilized cells, stepping external [Ca(2+)] from 0 to 3 μm also produced a larger [Ca(2+)]mito uptake in WT; moreover, the [Ca(2+)]mito uptake capacity of Bcl-xL-KO cells was restored by re-expression of mitochondrially targeted Bcl-xL. Bcl-xL enhancement of [Ca(2+)]mito uptake persisted after dissipation of the mitochondrial membrane potential but was absent in mitoplasts lacking an outer mitochondrial membrane. The outer membrane-localized voltage-dependent anion channel (VDAC) is a known Ca(2+) permeability pathway that directly interacts with Bcl-xL. Bcl-xL interacted with VDAC1 and -3 isoforms, and peptides based on the VDAC sequence disrupted Bcl-xL binding. Peptides reduced [Ca(2+)]mito uptake in WT but were without effect in Bcl-xL-KO cells. In addition, peptides reduced [Ca(2+)]mito uptake in VDAC1 and VDAC3 knock-out but not VDAC1 and -3 double knock-out mouse embryonic fibroblast cells, confirming that Bcl-xL interacts functionally with VDAC1 and -3 but not VDAC2. Thus, an interaction between Bcl-xL and VDAC promotes matrix Ca(2+) accumulation by increasing Ca(2+) transfer across the outer mitochondrial membrane.
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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.