ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Bax interacting factor-1 promotes survival and mitochondrial elongation in neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Alternative splicing fine-tunes modular protein interfaces to control protein localization.Nature structural & molecular biology · 2026Article
- Macrophage SH3 domain‑containing GRB2‑like protein B1 is required for Rab7‑mediated mitophagy in inflammation during sea water drowning acute lung injury.International journal of molecular medicine · 2026Article
- Comprehensive pan-cancer analysis reveals SH3GLB1 is a novel prognostic biomarker with immunomodulatory potential.Biology direct · 2026Article
- Endophilin B1 is essential for maintaining cardiac function by regulating mitocytosis.Cellular and molecular life sciences : CMLS · 2025Article
- Mitochondria are positioned at dendritic branch induction sites, a process requiring rhotekin2 and syndapin I.Nature communications · 2025Article
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Effect of Hydroxyurea on Morphology, Proliferation, and Protein Expression onInternational journal of molecular sciences · 2024Article
- Bif‑1 inhibits activation of inflammasome through autophagy regulatory mechanism.Molecular medicine reports · 2024Article
- Review
- Integrative Analysis of Machine Learning and Molecule Docking Simulations for Ischemic Stroke Diagnosis and Therapy.Molecules (Basel, Switzerland) · 2023Article
- Bif-1c Attenuates Viral Proliferation by Regulating Autophagic Flux Blockade Induced by the Rabies Virus CVS-11 Strain in N2a Cells.Microbiology spectrum · 2023Article
- Biology of endophilin and it's role in disease.Frontiers in immunology · 2023Review
- Reductions in Hydrogen Sulfide and Changes in Mitochondrial Quality Control Proteins Are Evident in the Early Phases of the Corneally Kindled Mouse Model of Epilepsy.International journal of molecular sciences · 2022Article
- Knock-Down of HDAC2 in Human Induced Pluripotent Stem Cell Derived Neurons Improves Neuronal Mitochondrial Dynamics, Neuronal Maturation and Reduces Amyloid Beta Peptides.International journal of molecular sciences · 2021Article
- Mitochondrial Quality Control: A Pathophysiological Mechanism and Therapeutic Target for Stroke.Frontiers in molecular neuroscience · 2021Review
- BIF-1 inhibits both mitochondrial and glycolytic ATP production: its downregulation promotes melanoma growth.Oncogene · 2020Article
- Neuronal susceptibility to beta-amyloid toxicity and ischemic injury involves histone deacetylase-2 regulation of endophilin-B1.Brain pathology (Zurich, Switzerland) · 2019Article
- Mitochondrial division inhibitor 1 protects cortical neurons from excitotoxicity: a mechanistic pathway.Neural regeneration research · 2018Article
- Tied up: Does altering phosphoinositide-mediated membrane trafficking influence neurodegenerative disease phenotypes?Journal of genetics · 2018Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Bax-interacting factor 1 (Bif-1, also known as endophilin B1) is a multifunctional protein involved in the regulation of apoptosis, mitochondrial morphology, and autophagy. Previous studies in non-neuronal cells have shown that Bif-1 is proapoptotic and promotes mitochondrial fragmentation. However, the role of Bif-1 in postmitotic neurons has not been investigated. In contrast to non-neuronal cells, we now report that in neurons Bif-1 promotes viability and mitochondrial elongation. In mouse primary cortical neurons, Bif-1 knockdown exacerbated apoptosis induced by the DNA-damaging agent camptothecin. Neurons from Bif-1-deficient mice contained fragmented mitochondria and Bif-1 knockdown in wild-type neurons also resulted in fragmented mitochondria which were more depolarized, suggesting mitochondrial dysfunction. During ischemic stroke, Bif-1 expression was downregulated in the penumbra of wild-type mice. Consistent with Bif-1 being required for neuronal viability, Bif-1-deficient mice developed larger infarcts and an exaggerated astrogliosis response following ischemic stroke. Together, these data suggest that, in contrast to non-neuronal cells, Bif-1 is essential for the maintenance of mitochondrial morphology and function in neurons, and that loss of Bif-1 renders neurons more susceptible to apoptotic stress. These unique actions may relate to the presence of longer, neuron-specific Bif-1 isoforms, because only these forms of Bif-1 were able to rescue deficiencies caused by Bif-1 suppression. This finding not only demonstrates an unexpected role for Bif-1 in the nervous system but this work also establishes Bif-1 as a potential therapeutic target for the treatment of neurological diseases, especially degenerative disorders characterized by alterations in mitochondrial dynamics.
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Registered trials
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