ArticleCell cycle (Georgetown, Tex.)2015
Metabolic epistasis among apoptosis-inducing factor and the mitochondrial import factor CHCHD4.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Enzymology of the metazoan tRNA ligase complex: a lifetime in cycles.Cellular and molecular life sciences : CMLS · 2026Review
- Mitochondrial innate immune signaling in skeletal muscle adaptation to exercise.Trends in endocrinology and metabolism: TEM · 2026Review
- CHCHD4 Oxidoreductase Activity: A Comprehensive Analysis of the Molecular, Functional, and Structural Properties of Its Redox-Regulated Substrates.Molecules (Basel, Switzerland) · 2025Review
- CHCHD4-TRIAP1 regulation of innate immune signaling mediates skeletal muscle adaptation to exercise.Cell reports · 2024Article
- Apoptosis-inducing factor: a mitochondrial protein associated with metabolic diseases-a narrative review.Cardiovascular diagnosis and therapy · 2023Review
- Cancer cell histone density links global histone acetylation, mitochondrial proteome and histone acetylase inhibitor sensitivity.Communications biology · 2022Article
- W196 and theOxidative medicine and cellular longevity · 2021Article
- Basal metabolic state governs AIF-dependent growth support in pancreatic cancer cells.BMC cancer · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypomorphic mutation of apoptosis-inducing factor (AIF) in the whole body or organ-specific knockout of AIF compromises the activity of respiratory chain complexes I and IV, as it confers resistance to obesity and diabetes induced by high-fat diet. The mitochondrial defect induced by AIF deficiency can be explained by reduced AIF-dependent mitochondrial import of CHCHD4, which in turn is required for optimal import and assembly of respiratory chain complexes. Here we show that, as compared to wild type control littermates, mice with a heterozygous knockout of CHCHD4 exhibit reduced weight gain when fed with a Western style high-fat diet. This finding suggests widespread metabolic epistasis among AIF and CHCHD4. Targeting either of these proteins or their functional interaction might constitute a novel strategy to combat obesity.
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