ArticleProceedings of the National Academy of Sciences of the United States of America2006
Loss of Aif function causes cell death in the mouse embryo, but the temporal progression of patterning is normal.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
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Who cites it
52 citing papers in PubMed, 99 citations in OpenAlex.
- Differential sensitivity of midline development to mitosis during and after primitive streak extension.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- AIF translocation into nucleus caused by Aifm1 R450Q mutation: generation and characterization of a mouse model for AUNX1.Human molecular genetics · 2024Article
- Apoptosis-inducing factor: a mitochondrial protein associated with metabolic diseases-a narrative review.Cardiovascular diagnosis and therapy · 2023Review
- A novel peptide encoded by N6-methyladenosine modified circMAP3K4 prevents apoptosis in hepatocellular carcinoma.Molecular cancer · 2022Article
- Cyclophilin D Regulates the Nuclear Translocation of AIF, Cardiac Endothelial Cell Necroptosis and Murine Cardiac Transplant Injury.International journal of molecular sciences · 2021Article
- Genetic mapping of renal glutathione suggests a novel regulatory locus on the murine X chromosome and overlap with hepatic glutathione regulation.Free radical biology & medicine · 2021Article
- Review
- OTUD1 Activates Caspase-Independent and Caspase-Dependent Apoptosis by Promoting AIF Nuclear Translocation and MCL1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Mitochondrial AIF loss causes metabolic reprogramming, caspase-independent cell death blockade, embryonic lethality, and perinatal hydrocephalus.Molecular metabolism · 2020Article
- The essentials of developmental apoptosis.F1000Research · 2020Review
- Reproductive functions of Kisspeptin/KISS1R Systems in the Periphery.Reproductive biology and endocrinology : RB&E · 2019Review
- AIF-regulated oxidative phosphorylation supports lung cancer development.Cell research · 2019Article
- AIF promotes a JNK1-mediated cadherin switch independently of respiratory chain stabilization.The Journal of biological chemistry · 2018Article
- Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis.Human molecular genetics · 2017Article
- GRIM-19: A master regulator of cytokine induced tumor suppression, metastasis and energy metabolism.Cytokine & growth factor reviews · 2017Review
- New protein-protein interactions of mitochondrial connexin 43 in mouse heart.Journal of cellular and molecular medicine · 2016Article
- Basal metabolic state governs AIF-dependent growth support in pancreatic cancer cells.BMC cancer · 2016Article
- Mitochondrial involvement in myocyte death and heart failure.Heart failure reviews · 2016Review
- Human anogenital distance: an update on fetal smoke-exposure and integration of the perinatal literature on sex differences.Human reproduction (Oxford, England) · 2016Article
- Apoptosis-Inducing-Factor-Dependent Mitochondrial Function Is Required for T Cell but Not B Cell Function.Immunity · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Apoptosis-inducing factor (AIF) is an evolutionarily conserved, ubiquitously expressed flavoprotein with NADH oxidase activity that is normally confined to mitochondria. In mammalian cells, AIF is released from mitochondria in response to apoptotic stimuli and translocates to the nucleus where it is thought to bind DNA and contribute to chromatinolysis and cell death in a caspase-independent manner. Here we describe the consequences of inactivating Aif in the early mouse embryo. Unexpectedly, we found that both the apoptosis-dependent process of cavitation in embryoid bodies and apoptosis associated with embryonic neural tube closure occur in the absence of AIF, indicating that Aif function is not required for apoptotic cell death in early mouse embryos. By embryonic day 9 (E9), loss of Aif function causes abnormal cell death, presumably because of reduced mitochondrial respiratory chain complex I activity. Because of this cell death, Aif null embryos fail to increase significantly in size after E9. Remarkably, patterning processes continue on an essentially normal schedule, such that E10 Aif null embryos with only approximately 1/10 the normal number of cells have the same somite number as their wild-type littermates. These observations show that pattern formation in the mouse can occur independent of embryo size and cell number.
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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.