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Telomere states and cell fates.

作者信息

Blackburn E H

机构信息

Department of Biochemistry and Microbiology, University of California, San Francisco 94143-0448, USA.

出版信息

Nature. 2000 Nov 2;408(6808):53-6. doi: 10.1038/35040500.

DOI:10.1038/35040500
PMID:11081503
Abstract
摘要

相似文献

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Telomere states and cell fates.端粒状态与细胞命运。
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Cell intrinsic and extrinsic mechanisms of stem cell aging depend on telomere status.干细胞衰老的细胞内在和外在机制取决于端粒状态。
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Genetics of proliferative aging.增殖性衰老的遗传学
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Senescence as an anticancer mechanism.衰老作为一种抗癌机制。
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Cellular responses to telomere shortening: cellular senescence as a tumor suppressor mechanism.细胞对端粒缩短的反应:细胞衰老作为一种肿瘤抑制机制。
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The role of NBS1 in DNA double strand break repair, telomere stability, and cell cycle checkpoint control.NBS1在DNA双链断裂修复、端粒稳定性及细胞周期检查点控制中的作用。
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ssDNA fragments induce cell senescence by telomere uncapping.单链DNA片段通过端粒解帽诱导细胞衰老。
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Cell senescence: hypertrophic arrest beyond the restriction point.细胞衰老:超越限制点的肥大性停滞。
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When CDK1 rides the telomere cycle.当细胞周期蛋白依赖性激酶1(CDK1)经历端粒循环时。
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Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors.衰老细胞、肿瘤抑制与机体衰老:良民,恶邻
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