ArticlePloS one2015
Phosphorylation of the BNIP3 C-Terminus Inhibits Mitochondrial Damage and Cell Death without Blocking Autophagy.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 68 citations in OpenAlex.
- Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure.JBMR plus · 2025Article
- Coordinating BNIP3/NIX-mediated mitophagy in space and time.Biochemical Society transactions · 2024Review
- Hypoxia-Preconditioned BMSC-Derived Exosomes Induce Mitophagy via the BNIP3-ANAX2 Axis to Alleviate Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Nix interacts with WIPI2 to induce mitophagy.The EMBO journal · 2023Article
- PPTC7 maintains mitochondrial protein content by suppressing receptor-mediated mitophagy.Nature communications · 2023Article
- Characteristics of glucose and lipid metabolism and the interaction between gut microbiota and colonic mucosal immunity in pigs during cold exposure.Journal of animal science and biotechnology · 2023Article
- Pptc7 maintains mitochondrial protein content by suppressing receptor-mediated mitophagy.bioRxiv : the preprint server for biology · 2023Article
- Role of mitophagy in the hallmarks of aging.Journal of biomedical research · 2022Article
- Hyperoxia Reprogrammes Microvascular Endothelial Cell Response to Hypoxia in an Organ-Specific Manner.Cells · 2022Article
- Article
- Hypoxia-Inducible Factors and Burn-Associated Acute Kidney Injury-A New Paradigm?International journal of molecular sciences · 2022Review
- Inhibition of the HIF-1 Survival Pathway as a Strategy to Augment Photodynamic Therapy Efficacy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Review
- Sequential perturbations to mouse corticogenesis following in utero maternal immune activation.eLife · 2021Article
- Iron Deficiency Reprograms Phosphorylation Signaling and Reduces O-GlcNAc Pathways in Neuronal Cells.Nutrients · 2021Article
- Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Research Progress on the Mechanism of Mitochondrial Autophagy in Cerebral Stroke.Frontiers in aging neuroscience · 2021Review
- Mitophagy and the Brain.International journal of molecular sciences · 2020Review
- BNIP3 in Lung Cancer: To Kill or Rescue?Cancers · 2020Review
- Autophagy markers as mediators of lung injury-implication for therapeutic intervention.Life sciences · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
BNIP3 is a dual function protein, able to activate autophagy and induce cell death. Upon expression of BNIP3, which is upregulated by hypoxia, the protein induces mitochondrial dysfunction, often leading to cell death. However, some highly respiring cells and cancer cells tolerate BNIP3 expression, suggesting that a yet unknown mechanism exists to restrain the lethal effects of BNIP3 on mitochondria. Here we present evidence that BNIP3 undergoes several phosphorylation events at its C-terminus, adjacent to the transmembrane domain. Phosphorylation at these residues inhibits BNIP3-induced mitochondrial damage, preventing a loss of mitochondrial mass and mitochondrial membrane potential, as well as preventing an increase in reactive oxygen species. This decrease in mitochondrial damage, as well as the reduction of cell death upon C-terminal BNIP3 phosphorylation, can be explained by a diminished interaction between BNIP3 and OPA1, a key regulator of mitochondrial fusion and mitochondrial inner membrane structure. Importantly, phosphorylation of these C-terminal BNIP3 residues blocks cell death without preventing autophagy, providing evidence that the two functional roles of BNIP3 can be regulated independently. These findings establish phosphorylation as a switch to determine the pro-survival and pro-death effects of the protein. Our findings also suggest a novel target for the regulation of these activities in transformed cells where BNIP3 is often highly expressed.
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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.