Transmitochondrial mice as models for primary prevention of diseases caused by mutation in the
<i>tRNA</i>
<sup>
<i>Lys</i>
</sup>
gene ([original](https://scite.ai/reports/24510903)) ([raw](?raw))
“…A transmitochondrial mouse with an m.7731G>A mutation in MT -TK (mitochondrial tRNA Lys ) gene was recently generated from a mouse lung carcinoma P29 cell line [ 10 ]. Mitochondrial transfer RNA (mt-tRNA) mutations are the most common mtDNA mutations to cause human disease, and this was the very fi rst mouse model with a point mutation in mitochondrial tRNA gene that has a counterpart in human patients affected by mitochondrial disease.…”
Section: Mt-tk Micementioning
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“…A transmitochondrial mouse with an m.7731G>A mutation in MT -TK (mitochondrial tRNA Lys ) gene was recently generated from a mouse lung carcinoma P29 cell line [ 10 ]. Mitochondrial transfer RNA (mt-tRNA) mutations are the most common mtDNA mutations to cause human disease, and this was the very fi rst mouse model with a point mutation in mitochondrial tRNA gene that has a counterpart in human patients affected by mitochondrial disease.…”
Section: Mt-tk Micementioning
“…Mitochondrial transfer RNA (mt-tRNA) mutations are the most common mtDNA mutations to cause human disease, and this was the very fi rst mouse model with a point mutation in mitochondrial tRNA gene that has a counterpart in human patients affected by mitochondrial disease. The mice were created by fusing ES cells depleted of mitochondria with the cybrid clone having 70 % heteroplasmy for MT -TK m.7731G>A [ 10 ]. The mutation was transmitted through subsequent generations, if present in ≤85 % heteroplasmy, while oocytes containing a higher mutational load seem to be lost during development [ 10 ].…”
Section: Mt-tk Micementioning
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“…The first transmitochondrial mouse carrying a point mutation in tRNA Lys gene was generated very recently by selecting a tRNA mutation by PCR screening of somatic variants occurring in mouse lung carcinoma P29 cells (Shimizu, 2014). The G7731A mutation was highly conserved among the species and had a counterpart in human mtDNA from patients affected by mitochondrial disease.…”
Section: Mouse Models Of Mtdna Mutations In Oxphos Subunits and Trmentioning