Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne 1015, Switzerland.
Institute of Molecular Biology, Academia Sinica, 128 Academia Road, Section 2, Taipei 11529, Taiwan.
Trends Biochem Sci. 2015 May;40(5):275-85. doi: 10.1016/j.tibs.2015.03.003. Epub 2015 Apr 3.
Telomeres are nucleoprotein structures capping the natural termini of eukaryotic linear chromosomes. Telomeres possess an inherent ability to circumvent the activation of a full-blown DNA damage response (DDR), and hence fusion reactions, by limiting inappropriate double-strand break (DSB) repair and processing activities at eukaryotic chromosome ends. A telomere-specific protein complex, termed shelterin, has a crucial function in safeguarding and securing telomere integrity. Within this complex, TRF2 has emerged as the key player, dictating different states of telomere protection during the replicative lifespan of a cell. How TRF2 prevents activation of DSB repair activities at functional telomeres has now been extensively investigated. In this review we aim at exploring the complex and multi-faceted mechanisms underlying the TRF2-mediated protection of eukaryotic chromosome ends.
端粒是真核线性染色体自然末端的核蛋白结构。端粒具有规避全面 DNA 损伤反应 (DDR) 的固有能力，因此通过限制真核染色体末端不合适的双链断裂 (DSB) 修复和处理活性来避免融合反应。一种称为 shelterin 的端粒特异性蛋白复合物在保护和确保端粒完整性方面具有关键作用。在这个复合物中，TRF2 已经成为关键的参与者，决定了细胞复制寿命中端粒保护的不同状态。TRF2 如何防止在功能端粒处激活 DSB 修复活性已被广泛研究。在这篇综述中，我们旨在探索 TRF2 介导的真核染色体末端保护的复杂和多方面的机制。
