ArticleThe Journal of biological chemistry2014
Plasminogen kringle 5 induces endothelial cell apoptosis by triggering a voltage-dependent anion channel 1 (VDAC1) positive feedback loop.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- The compartment-specific interactome of VDAC1 reveals its emerging role beyond mitochondria in breast cancer.Scientific reports · 2026Article
- The Pathophysiological Role of Mitochondria-associated Membranes in Coronary Artery Disease and Atherosclerosis.Current medicinal chemistry · 2026Review
- AAV for ovarian cancer gene therapy.Cancer gene therapy · 2025Review
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Review
- Inhibition of extranodal NK/T-cell lymphoma by Chiauranib through an AIF-dependent pathway and its synergy with L-asparaginase.Cell death & disease · 2023Article
- Accumulation of Fat Not Responsible for Femoral Head Necrosis, Revealed by Single-Cell RNA Sequencing: A Preliminary Study.Biomolecules · 2023Article
- Ceramide Kinase Inhibition Drives Ferroptosis and Sensitivity to Cisplatin in Mutant KRAS Lung Cancer by Dysregulating VDAC-Mediated Mitochondria Function.Molecular cancer research : MCR · 2022Article
- α2-Antiplasmin as a Potential Therapeutic Target for Systemic Sclerosis.Life (Basel, Switzerland) · 2022Review
- Response Predictive Markers and Synergistic Agents for Drug Repositioning of Statins in Ovarian Cancer.Pharmaceuticals (Basel, Switzerland) · 2022Article
- A functional outside-in signaling network of proteoglycans and matrix molecules regulating autophagy.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Antiangiogenic therapy in diabetic nephropathy: A double‑edged sword (Review).Molecular medicine reports · 2021Review
- Mapping transmembrane binding partners for E-cadherin ectodomains.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases.Biomolecules · 2020Review
- Elevated pigment epithelium-derived factor induces diabetic erectile dysfunction via interruption of the Akt/Hsp90β/eNOS complex.Diabetologia · 2020Article
- Alterations in the chondrocyte surfaceome in response to pro-inflammatory cytokines.BMC molecular and cell biology · 2020Article
- miR-197-3p Represses the Proliferation of Prostate Cancer by Regulating the VDAC1/AKT/β-catenin Signaling Axis.International journal of biological sciences · 2020Article
- The Role of Fibrinolytic Regulators in Vascular Dysfunction of Systemic Sclerosis.International journal of molecular sciences · 2019Review
- LncRNA HULC Polymorphism Is Associated With Recurrent Spontaneous Abortion Susceptibility in the Southern Chinese Population.Frontiers in genetics · 2019Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human plasminogen kringle 5 (K5) is known to display its potent anti-angiogenesis effect through inducing endothelial cell (EC) apoptosis, and the voltage-dependent anion channel 1 (VDAC1) has been identified as a receptor of K5. However, the exact role and underlying mechanisms of VDAC1 in K5-induced EC apoptosis remain elusive. In the current study, we showed that K5 increased the protein level of VDAC1, which initiated the mitochondrial apoptosis pathway of ECs. Our findings also showed that K5 inhibited the ubiquitin-dependent degradation of VDAC1 by promoting the phosphorylation of VDAC1, possibly at Ser-12 and Thr-107. The phosphorylated VDAC1 was attenuated by the AKT agonist, glycogen synthase kinase (GSK) 3β inhibitor, and siRNA, suggesting that K5 increased VDAC1 phosphorylation via the AKT-GSK3β pathway. Furthermore, K5 promoted cell surface translocation of VDAC1, and binding between K5 and VDAC1 was observed on the plasma membrane. HKI protein blocked the impact of K5 on the AKT-GSK3β pathway by competitively inhibiting the interaction of K5 and cell surface VDAC1. Moreover, K5-induced EC apoptosis was suppressed by VDAC1 antibody. These data show for the first time that K5-induced EC apoptosis is mediated by the positive feedback loop of "VDAC1-AKT-GSK3β-VDAC1," which may provide new perspectives on the mechanisms of K5-induced apoptosis.
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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.