作者: Hayden A. Homer
DOI: 10.14670/HH-21.873
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摘要: During mammalian mitosis, a proofreading network called the spindle assembly checkpoint (SAC) is indispensable for ensuring fidelity of chromosome segregation. An inhibitory SAC signal deputed to inhibits mitotic cell-cycle progression in response misaligned chromosomes until such imperfections are rectified thereby equitable partitioning daughter cells. Amongst cast proteins, arrest deficient 2 (Mad2) plays leading role transducing signal. The aneuploidy and cancer predispositions individuals who harbour genetic mutations genes emphasise vivo significance this surveillance mechanism. In humans, congenital aneuploidies as Down's syndrome demonstrate an exponential increase with advancing female age. Although largely result meiosis I errors, molecular entities that succumb age oocytes remain elusive. Declining oocyte function could plausibly contribute errors. Until recently however, convincing evidence functional during was unforthcoming. Here review regarding how our understanding system has evolved recent years. This will focus on Mad2 protein been most comprehensively investigated.