ArticleGenes & development2015
Loss of the RNA polymerase III repressor MAF1 confers obesity resistance.
Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 120 citations in OpenAlex.
- Identification of novel candidate neural genes for diet-induced obesity in outbred heterogeneous stock rats.Research square · 2026Article
- Loss of Pol III repressor Maf1 in neurons promotes longevity by preventing the age-related decline in 5S rRNA and translation.PLoS biology · 2025Article
- Article
- Molecular basis of neurodegeneration in a mouse model ofbioRxiv : the preprint server for biology · 2024Article
- Maf1 loss regulates spinogenesis and attenuates cognitive impairment in Alzheimer's disease.Brain : a journal of neurology · 2024Article
- Engineered mischarged transfer RNAs for correcting pathogenic missense mutations.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Review
- Emerging role of lipophagy in liver disorders.Molecular and cellular biochemistry · 2024Review
- Selective gene expression maintains human tRNA anticodon pools during differentiation.Nature cell biology · 2024Article
- Polyamines: their significance for maintaining health and contributing to diseases.Cell communication and signaling : CCS · 2023Review
- Promoting metabolic inefficiency for metabolic disease.iScience · 2023Review
- Maf1 is an intrinsic suppressor against spontaneous neural repair and functional recovery after ischemic stroke.Journal of advanced research · 2023Article
- Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis.Nucleic acids research · 2023Article
- RNA Polymerases I and III in development and disease.Seminars in cell & developmental biology · 2023Review
- SLC3A2 and SLC7A2 Mediate the Exogenous Putrescine-Induced Adipocyte Differentiation.Molecules and cells · 2022Article
- A Polymorphism in the Gene Encoding Heat Shock Factor 1 (Life (Basel, Switzerland) · 2022Article
- Oral Supplementation with the Polyamine Spermidine Affects Hepatic but Not Pulmonary Lipid Metabolism in Lean but Not Obese Mice.Nutrients · 2022Article
- Article
- Differential release of extracellular vesicle tRNA from oxidative stressed renal cells and ischemic kidneys.Scientific reports · 2022Article
- New Insights into the Roles and Mechanisms of Spermidine in Aging and Age-Related Diseases.Aging and disease · 2021Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
Abstract
MAF1 is a global repressor of RNA polymerase III transcription that regulates the expression of highly abundant noncoding RNAs in response to nutrient availability and cellular stress. Thus, MAF1 function is thought to be important for metabolic economy. Here we show that a whole-body knockout of Maf1 in mice confers resistance to diet-induced obesity and nonalcoholic fatty liver disease by reducing food intake and increasing metabolic inefficiency. Energy expenditure in Maf1(-/-) mice is increased by several mechanisms. Precursor tRNA synthesis was increased in multiple tissues without significant effects on mature tRNA levels, implying increased turnover in a futile tRNA cycle. Elevated futile cycling of hepatic lipids was also observed. Metabolite profiling of the liver and skeletal muscle revealed elevated levels of many amino acids and spermidine, which links the induction of autophagy in Maf1(-/-) mice with their extended life span. The increase in spermidine was accompanied by reduced levels of nicotinamide N-methyltransferase, which promotes polyamine synthesis, enables nicotinamide salvage to regenerate NAD(+), and is associated with obesity resistance. Consistent with this, NAD(+) levels were increased in muscle. The importance of MAF1 for metabolic economy reveals the potential for MAF1 modulators to protect against obesity and its harmful consequences.
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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.