ArticleMethods in molecular biology (Clifton, N.J.)2012
Molecular profiling of mitochondrial dysfunction in Caenorhabditis elegans.
Article in Methods in molecular biology (Clifton, N.J.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed.
- The Juvenile Parkinson's Disease Mutation C212Y Impairs Mitochondrial Homeostasis in a Caenorhabditis elegans Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- ULP-2 SUMO protease regulates UPRFree radical biology & medicine · 2024Article
- Combinatorial glucose, nicotinic acid and N-acetylcysteine therapy has synergistic effect in preclinical C. elegans and zebrafish models of mitochondrial complex I disease.Human molecular genetics · 2021Article
- Comparative Analysis of Experimental Methods to Quantify Animal Activity in Caenorhabditis elegans Models of Mitochondrial Disease.Journal of visualized experiments : JoVE · 2021Article
- Pre-clinical evaluation of cysteamine bitartrate as a therapeutic agent for mitochondrial respiratory chain disease.Human molecular genetics · 2019Article
- N-acetylcysteine and vitamin E rescue animal longevity and cellular oxidative stress in pre-clinical models of mitochondrial complex I disease.Molecular genetics and metabolism · 2018Article
- Multiple Molecular Mechanisms Rescue mtDNA Disease in C. elegans.Cell reports · 2018Article
- Cell Biology of the Mitochondrion.Genetics · 2017Review
- Inhibiting cytosolic translation and autophagy improves health in mitochondrial disease.Human molecular genetics · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Cellular effects of primary mitochondrial dysfunction, as well as potential mitochondrial disease therapies, can be modeled in living animals such as the microscopic nematode, Caenorhabditis elegans. In particular, molecular analyses can provide substantial insight into the mechanism by which genetic and/or pharmacologic manipulations alter mitochondrial function. The relative expression of individual genes across both nuclear and mitochondrial genomes, as well as relative quantitation of mitochondrial DNA content, can be readily performed by quantitative real-time PCR (qRT-PCR) analysis of C. elegans. Additionally, microarray expression profiling offers a powerful tool by which to survey the global genetic consequences of various causes of primary mitochondrial dysfunction and potential therapeutic interventions at both the single gene and integrated pathway level. Here, we describe detailed protocols for RNA and DNA isolation from whole animal populations in C. elegans, qRT-PCR analysis of both nuclear and mitochondrial genes, and global nuclear genome expression profiling using the Affymetrix GeneChip C. elegans Genome Array.
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Registered trials
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