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Shelterin complex and associated factors at human telomeres

机译：人端粒中的Shelterin复合体和相关因素

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The processes regulating telomere function have major impacts on fundamental issues in human cancer biology. First, active telomere maintenance is almost always required for full oncogenic transformation of human cells, through cellular immortalization by endowment of an infinite replicative potential. Second, the attrition that telomeres undergo upon replication is responsible for the finite replicative life span of cells in culture, a process called senescence, which is of paramount importance for tumor suppression in vivo. The process of telomere-based senescence is intimately coupled to the induction of a DNA damage response emanating from telomeres, which can be elicited by both the ATM and ATR dependent pathways. At telomeres, the shelterin complex is constituted by a group of six proteins which assembles quantitatively along the telomere tract, and imparts both telomere maintenance and telomere protection. Shelterin is known to regulate the action of telomerase, and to prevent inappropriate DNA damage responses at chromosome ends, mostly through inhibition of ATM and ATR. The roles of shelterin have increasingly been associated with transient interactions with downstream factors that are not associated quantitatively or stably with telomeres. Here, some of the important known interactions between shelterin and these associated factors and their interplay to mediate telomere functions are reviewed.
机译：调节端粒功能的过程对人类癌症生物学的基本问题具有重大影响。首先，通过赋予无限复制潜力使细胞永生化，几乎总是需要主动端粒维持来实现人类细胞的完全致癌转化。第二，端粒复制时的损耗是培养细胞有限复制寿命的原因，这一过程称为衰老，这对于体内肿瘤抑制至关重要。基于端粒的衰老过程与端粒产生的DNA损伤反应的诱导密切相关，这可以通过ATM和ATR依赖性途径引发。在端粒中，庇护蛋白复合物由沿着端粒定量组装的六种蛋白质组成，既赋予了端粒维持能力，又赋予了端粒保护功能。众所周知，Shelterin调节端粒酶的作用，并通过主要抑制ATM和ATR来防止染色体末端的不适当的DNA损伤反应。遮蔽蛋白的作用越来越与与下游因子的瞬时相互作用相关，而下游因子在数量上或与端粒没有稳定地关联。在这里，审查了掩蔽蛋白和这些相关因素之间的一些重要的已知相互作用及其介导端粒功能的相互作用。

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