ArticleThe EMBO journal2006
Dissociating the dual roles of apoptosis-inducing factor in maintaining mitochondrial structure and apoptosis.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 191 citations in OpenAlex.
- Mitochondrial Fission Regulator 1-Like Protein Protects the Heart from Ischemia/Reperfusion Injury via Dual Mitochondrial Mechanisms.Research (Washington, D.C.) · 2026Article
- Dietary lipid content modifies wah-1/AIFM1-associated phenotypes via LRK-1 and DRP-1 expression in C. elegans.Nature communications · 2025Article
- Exploring the role of parthanatos in CNS injury: Molecular insights and therapeutic approaches.Journal of advanced research · 2025Review
- AIF3 splicing variant elicits mitochondrial malfunction via the concurrent dysregulation of electron transport chain and glutathione-redox homeostasis.Nature communications · 2025Article
- Exploring genetic associations and drug targets for mitochondrial proteins and schizophrenia risk.Schizophrenia (Heidelberg, Germany) · 2025Article
- Parthanatos: Mechanisms, modulation, and therapeutic prospects in neurodegenerative disease and stroke.Biochemical pharmacology · 2024Review
- AIF translocation into nucleus caused by Aifm1 R450Q mutation: generation and characterization of a mouse model for AUNX1.Human molecular genetics · 2024Article
- Targeting the Metabolic Paradigms in Cancer and Diabetes.Biomedicines · 2024Review
- Expanding the spectrum of neonatal-onset AIFM1-associated disorders.Annals of clinical and translational neurology · 2023Article
- Apoptosis-inducing factor: a mitochondrial protein associated with metabolic diseases-a narrative review.Cardiovascular diagnosis and therapy · 2023Review
- Impaired AIF-CHCHD4 interaction and mitochondrial calcium overload contribute to auditory neuropathy spectrum disorder in patient-iPSC-derived neurons with AIFM1 variant.Cell death & disease · 2023Article
- Article
- Ubiquitinated AIF is a major mediator of hypoxia-induced mitochondrial dysfunction and pulmonary artery smooth muscle cell proliferation.Cell & bioscience · 2022Article
- The key players of parthanatos: opportunities for targeting multiple levels in the therapy of parthanatos-based pathogenesis.Cellular and molecular life sciences : CMLS · 2022Review
- Relevance of AIF/CypA Lethal Pathway in SH-SY5Y Cells Treated with Staurosporine.International journal of molecular sciences · 2021Article
- Molecular characterization of a complex of apoptosis-inducing factor 1 with cytochrome c oxidase of the mitochondrial respiratory chain.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- AIF3 splicing switch triggers neurodegeneration.Molecular neurodegeneration · 2021Article
- OTUD1 Activates Caspase-Independent and Caspase-Dependent Apoptosis by Promoting AIF Nuclear Translocation and MCL1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- An antibody toolbox to track complex I assembly defines AIF's mitochondrial function.The Journal of cell biology · 2020Article
- Mitochondrial AIF loss causes metabolic reprogramming, caspase-independent cell death blockade, embryonic lethality, and perinatal hydrocephalus.Molecular metabolism · 2020Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial protein apoptosis-inducing factor (AIF) translocates to the nucleus and induces apoptosis. Recent studies, however, have indicated the importance of AIF for survival in mitochondria. In the absence of a means to dissociate these two functions, the precise roles of AIF remain unclear. Here, we dissociate these dual roles using mitochondrially anchored AIF that cannot be released during apoptosis. Forebrain-specific AIF null (tel. AifDelta) mice have defective cortical development and reduced neuronal survival due to defects in mitochondrial respiration. Mitochondria in AIF deficient neurons are fragmented with aberrant cristae, indicating a novel role of AIF in controlling mitochondrial structure. While tel. AifDelta Apaf1(-/-) neurons remain sensitive to DNA damage, mitochondrially anchored AIF expression in these cells significantly enhanced survival. AIF mutants that cannot translocate into nucleus failed to induce cell death. These results indicate that the proapoptotic role of AIF can be uncoupled from its physiological function. Cell death induced by AIF is through its proapoptotic activity once it is translocated to the nucleus, not due to the loss of AIF from the mitochondria.
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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.