ReviewAntioxidants & redox signaling2011
Mechanisms and biology of B-cell leukemia/lymphoma 2/adenovirus E1B interacting protein 3 and Nip-like protein X.
Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Pexophagy and Oxidative Stress: Focus on Peroxisomal Proteins and Reactive Oxygen Species (ROS) Signaling Pathways.Antioxidants (Basel, Switzerland) · 2025Review
- Mitophagy in Cell Death Regulation: Insights into Mechanisms and Disease Implications.Biomolecules · 2024Review
- Review
- The dual roles of autophagy and the GPCRs-mediating autophagy signaling pathway after cerebral ischemic stroke.Molecular brain · 2022Review
- Perspectives on mitochondrial relevance in cardiac ischemia/reperfusion injury.Frontiers in cell and developmental biology · 2022Review
- BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease.Cell death & disease · 2021Review
- Exercise-Induced Benefits for Alzheimer's Disease by Stimulating Mitophagy and Improving Mitochondrial Function.Frontiers in aging neuroscience · 2021Review
- Mitophagy in Diabetic Cardiomyopathy: Roles and Mechanisms.Frontiers in cell and developmental biology · 2021Review
- Mitophagy in Cardiovascular Diseases.Journal of clinical medicine · 2020Review
- DNA methylation of the promoter region of bnip3 and bnip3l genes induced by metabolic programming.BMC genomics · 2018Article
- BNIP3L/NIX is required for elimination of mitochondria, endoplasmic reticulum and Golgi apparatus during eye lens organelle-free zone formation.Experimental eye research · 2018Article
- Protective roles of autophagy in retinal pigment epithelium under high glucose condition via regulating PINK1/Parkin pathway and BNIP3L.Biological research · 2018Article
- Autophagy in Traumatic Brain Injury: A New Target for Therapeutic Intervention.Frontiers in molecular neuroscience · 2018Review
- Expression and Functional Characterization of the BNIP3 Protein in Renal Cell Carcinomas.Translational oncology · 2017Article
- Insulin-like growth factor 1 signaling is essential for mitochondrial biogenesis and mitophagy in cancer cells.The Journal of biological chemistry · 2017Article
- BNIP3L in myelodysplastic syndromes and acute myeloid leukemia: impact on disease outcome and cellular response to decitabine.Haematologica · 2016Article
- Novel p53-dependent anticancer strategy by targeting iron signaling and BNIP3L-induced mitophagy.Oncotarget · 2016Article
- Bnip3 Binds and Activates p300: Possible Role in Cardiac Transcription and Myocyte Morphology.PloS one · 2015Article
- p53 and mitochondrial function in neurons.Biochimica et biophysica acta · 2014Review
- Autophagy: a double-edged sword for neuronal survival after cerebral ischemia.Neural regeneration research · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
B-cell leukemia/lymphoma 2 (BCL-2)/adenovirus E1B interacting protein 3 (BNIP3) and Nip-like protein X (NIX) are atypical BCL-2 homology domain 3-only proteins involved in cell death, autophagy, and programmed mitochondrial clearance. BNIP3 and NIX cause cell death by targeting mitochondria, directly through BCL-2-associated X protein- or BCL-2-antagonist/killer-dependent mechanisms, or indirectly through an effect on calcium stores in the endoplasmic reticulum. BNIP3 and NIX also induce autophagy through an effect on mitochondrial reactive oxygen species production, or by releasing Beclin 1 from inhibitory interactions with antiapoptotic BCL-2 family proteins. BNIP3 downregulates mitochondrial mass in hypoxic cells, whereas NIX is required for mitochondrial elimination during erythroid development. BNIP3 and NIX have an emerging role in human health. Cell death mediated by BNIP3 and NIX is implicated in heart disease and ischemic injury. Cancer progression is linked to loss of the prodeath function of BNIP3, but also to induction of its prosurvival activity. Finally, BNIP3 and NIX are implicated in mitochondrial quality control, which is important in aging and degenerative disease. Elucidation of the mechanisms by which BNIP3 and NIX regulate cell death, autophagy, and mitochondrial clearance may lead to treatments for these conditions.
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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.