ArticleMitochondrion2011
Xenomitochondrial mice: investigation into mitochondrial compensatory mechanisms.
Article in Mitochondrion, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed.
- Recent Advances in Mitochondrial Transplantation for Ischemic Stroke: A Review of in Vitro and in Vivo Studies.Translational stroke research · 2026Review
- Preclinical models of mitochondrial dysfunction: mtDNA and nuclear-encoded regulators in diverse pathologies.Frontiers in aging · 2025Review
- Nuclear response to divergent mitochondrial DNA genotypes modulates the interferon immune response.PloS one · 2020Article
- Artificial Mitochondria Transfer: Current Challenges, Advances, and Future Applications.Stem cells international · 2017Review
- Mitochondrial transfer: Implications for assisted reproductive technologies.Applied & translational genomics · 2016Review
- Incompatibility between Nuclear and Mitochondrial Genomes Contributes to an Interspecies Reproductive Barrier.Cell metabolism · 2016Article
- Mitochondrial DNA disease and developmental implications for reproductive strategies.Molecular human reproduction · 2015Review
- The emergence of the mitochondrial genome as a partial regulator of nuclear function is providing new insights into the genetic mechanisms underlying age-related complex disease.Human genetics · 2014Review
- The challenges of mitochondrial replacement.PLoS genetics · 2014Article
- Mitochondrial abnormalities in temporal lobe of autistic brain.Neurobiology of disease · 2013Article
- Reprogramming and development in nuclear transfer embryos and in interspecific systems.Current opinion in genetics & development · 2012Review
- On the cellular and developmental lethality of a Xenopus nucleocytoplasmic hybrid.Communicative & integrative biology · 2012Article
- Animal models of human mitochondrial DNA mutations.Biochimica et biophysica acta · 2012Review
- Amphibian interorder nuclear transfer embryos reveal conserved embryonic gene transcription, but deficient DNA replication or chromosome segregation.The International journal of developmental biology · 2012Article
- Evolution of the couple cytochrome c and cytochrome c oxidase in primates.Advances in experimental medicine and biology · 2012Review
- Mitochondrial biology in reproduction.Reproductive medicine and biology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Xenomitochondrial mice, harboring evolutionarily divergent Mus terricolor mitochondrial DNA (mtDNA) on a Mus musculus domesticus nuclear background (B6NTac(129S6)-mt(M. terricolor)/Capt; line D7), were subjected to molecular and phenotypic analyses. No overt in vivo phenotype was identified in contrast to in vitro xenomitochondrial cybrid studies. Microarray analyses revealed differentially expressed genes in xenomitochondrial mice, though none were directly involved in mitochondrial function. qRT-PCR revealed upregulation of mt-Co2 in xenomitochondrial mice. These results illustrate that cellular compensatory mechanisms for mild mitochondrial dysfunction alter mtDNA gene expression at a proteomic and/or translational level. Understanding these mechanisms will facilitate the development of therapeutics for mitochondrial disorders.
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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.