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Showing 1–7 of 7 results
Advanced filters: Author: Michelle Sparman Clear advanced filters

  • The mitochondrial genome is of maternal origin and mutations in mitochondrial DNA are the cause of many human diseases. The efficient replacement of the mitochondrial genome in mature non-human primate oocytes is now demonstrated. This approach may offer a reproductive option to prevent the transmission of diseases caused by mutations in mitochondrial DNA in affected families.

    • Masahito Tachibana
    • Michelle Sparman
    • Shoukhrat Mitalipov
    Research
    Nature
    Volume: 461, P: 367-372

  • Genome-wide analysis of matched human IVF embryonic stem cells (IVF ES cells), induced pluripotent stem cells (iPS cells) and nuclear transfer ES cells (NT ES cells) derived by somatic cell nuclear transfer (SCNT) reveals that human somatic cells can be faithfully reprogrammed to pluripotency by SCNT; NT ES cells and iPS cells derived from the same somatic cells contain comparable numbers of de novo copy number variations, but whereas DNA methylation and transcriptome profiles of NT ES cells and IVF ES cells are similar, iPS cells have residual patterns typical of parental somatic cells.

    • Hong Ma
    • Robert Morey
    • Shoukhrat Mitalipov
    Research
    Nature
    Volume: 511, P: 177-183

  • Mutations in mitochondrial DNA cause a wide range of disorders in humans, with a high prevalence; here it is shown that the nucleus of an affected woman’s egg could be inserted into healthy donor egg cytoplasm by spindle transfer, allowing the birth of healthy offspring.

    • Masahito Tachibana
    • Paula Amato
    • Shoukhrat Mitalipov
    Research
    Nature
    Volume: 493, P: 627-631

  • Reprogramming after somatic cell nuclear transfer had been thought to be dependent on the recipient cytoplasm being arrested at the metaphase stage, but here interphase two-cell mouse embryos are shown to support successful reprogramming and generation of embryonic stem cells or cloned mice.

    • Eunju Kang
    • Guangming Wu
    • Shoukhrat Mitalipov
    Research
    Nature
    Volume: 509, P: 101-104