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结果能证明手段合理吗?:端粒与哺乳动物细胞复制性衰老和永生化的机制

Can ends justify the means?: telomeres and the mechanisms of replicative senescence and immortalization in mammalian cells.

作者信息

Sedivy J M

机构信息

Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02912, USA.

出版信息

Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9078-81. doi: 10.1073/pnas.95.16.9078.

Abstract

Finite replicative lifespan, or senescence, of mammalian cells in culture is a phenomenon that has generated much curiosity since its description. The obvious significance of senescence to organismal aging and the development of cancer has engendered a long-lasting and lively debate about its mechanisms. Recent discoveries concerning the phenotypes of telomerase knockout mice, the consequences of telomerase reexpression in somatic cells, and genes that regulate senescence have provided striking molecular insights but also have uncovered important new questions. The objective of this review is to reconcile old observations with new molecular details and to focus attention on the key remaining puzzles.

摘要

培养的哺乳动物细胞的有限复制寿命,即衰老,自被描述以来一直是一种引发诸多好奇的现象。衰老对机体衰老和癌症发展的明显意义引发了关于其机制的长期而热烈的争论。最近有关端粒酶敲除小鼠的表型、体细胞中端粒酶重新表达的后果以及调节衰老的基因的发现,不仅提供了引人注目的分子见解,也揭示了重要的新问题。本综述的目的是将旧的观察结果与新的分子细节相协调,并将注意力集中在剩下的关键谜题上。

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本文引用的文献

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The Fusion of Broken Ends of Chromosomes Following Nuclear Fusion.核融合后染色体断端的融合
Proc Natl Acad Sci U S A. 1942 Nov;28(11):458-63. doi: 10.1073/pnas.28.11.458.
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Role of the p16 tumor suppressor gene in cancer.p16肿瘤抑制基因在癌症中的作用。
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