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Times Cited: 181
Times Cited
Times Co-cited
Similarity
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A mouse model of mitochondrial disease reveals germline selection against severe mtDNA mutations.
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Extensive tissue-related and allele-related mtDNA heteroplasmy suggests positive selection for somatic mutations.
Mingkun Li, Roland Schröder, Shengyu Ni, Burkhard Madea, Mark Stoneking. Proc Natl Acad Sci U S A 2015
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Random genetic drift in the female germline explains the rapid segregation of mammalian mitochondrial DNA.
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The mitochondrial DNA genetic bottleneck results from replication of a subpopulation of genomes.
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Specific elimination of mutant mitochondrial genomes in patient-derived cells by mitoTALENs.
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A reduction of mitochondrial DNA molecules during embryogenesis explains the rapid segregation of genotypes.
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Mitochondrial aging is accelerated by anti-retroviral therapy through the clonal expansion of mtDNA mutations.
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Somatic progenitor cell vulnerability to mitochondrial DNA mutagenesis underlies progeroid phenotypes in Polg mutator mice.
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Random point mutations with major effects on protein-coding genes are the driving force behind premature aging in mtDNA mutator mice.
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Mitochondrial diseases.
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Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice.
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A Phenotype-Driven Approach to Generate Mouse Models with Pathogenic mtDNA Mutations Causing Mitochondrial Disease.
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Segregation of mitochondrial DNA heteroplasmy through a developmental genetic bottleneck in human embryos.
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Variation in germline mtDNA heteroplasmy is determined prenatally but modified during subsequent transmission.
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8
Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.