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摘要: The molecular regulation of telomere length has been well elucidated by a series elegant studies over the past decade. More recently, experimental evidence accrued that addresses challenging question if and how may contribute to normal human aging or disease. Recent in mice have provided mammalian precedent indicating telomerase deficiency can lead vivo dysfunction, most probably as consequence progressive shortening. In humans, shortening might dysfunction is far less direct, although recent description associated with DKC syndrome suggestive such link. Methodologies exist continue be developed are increasingly capable manipulating activity cells. It remains determined whether scientifically rigorous (equally important) medically ethical approaches will emerge directly assess ability modulation correct functional disorders cellular function ex or, more still, vivo.