The Journal of nutritional biochemistry · 2003
Folate deficiency, mismatch repair-dependent apoptosis, and human disease.
СтатьяПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Guo Min, Presnell Steven R, Gu Liya
Аннотация
The vitamin that is most commonly deficient in the American diet is folate. Severe folate deficiency in humans is known to cause megaloblastic anemia and developmental defects, and is associated with an increased incidence of several forms of human cancer. Although the exact mechanisms by which this vitamin deficiency may cause these diseases are not known at the present time, recent work has shown that folate deficiency also causes genomic instability and programmed cell death (or apoptosis). Additionally, it is known that the DNA mismatch repair pathway mediates folate deficiency-induced apoptosis. This review will first describe work suggesting that folate deficiency causes genomic instability and apoptosis, then discuss possible mechanisms by which the mismatch repair pathway could trigger folate deficiency-induced apoptosis, which has either protective or destructive effects on tissue.