ATRX dysfunction induces replication defects in primary mouse cells.
ATRX dysfunction induces replication defects in primary mouse cells.
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DOI：
10.1371/journal.pone.0092915
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Gibbons RJ
中科院分区：
文献类型：
--
作者：
Clynes D;Jelinska C;Xella B;Ayyub H;Taylor S;Mitson M;Bachrati CZ;Higgs DR;Gibbons RJ
染色质重塑蛋白 ATRX 以串联重复 DNA 为靶点，已被证明是 α 球蛋白基因的表达、各种细胞祖细胞的增殖、染色体会聚和端粒维持所必需的。最近在肿瘤中发现了 ATRX 突变，这些突变通过端粒酶独立途径维持其端粒，该途径涉及被认为由 DNA 损伤触发的同源重组。目前尚不清楚是否存在与 ATRX 功能障碍相关的核心潜在机制，该机制可以解释观察到的众多细胞现象。然而，越来越多的证据表明它在各种重复 DNA 模板的复制中发挥作用，这些重复 DNA 模板被认为具有形成二级结构的倾向。使用小鼠基因敲除模型，我们证明 ATRX 在促进 DNA 复制中发挥直接作用。单独消除 ATRX 虽然会导致端粒 DNA 损伤反应，但不足以触发小鼠胚胎干细胞中端粒途径的替代性延长。
The chromatin remodeling protein ATRX, which targets tandem repetitive DNA, has been shown to be required for expression of the alpha globin genes, for proliferation of a variety of cellular progenitors, for chromosome congression and for the maintenance of telomeres. Mutations in ATRX have recently been identified in tumours which maintain their telomeres by a telomerase independent pathway involving homologous recombination thought to be triggered by DNA damage. It is as yet unknown whether there is a central underlying mechanism associated with ATRX dysfunction which can explain the numerous cellular phenomena observed. There is, however, growing evidence for its role in the replication of various repetitive DNA templates which are thought to have a propensity to form secondary structures. Using a mouse knockout model we demonstrate that ATRX plays a direct role in facilitating DNA replication. Ablation of ATRX alone, although leading to a DNA damage response at telomeres, is not sufficient to trigger the alternative lengthening of telomere pathway in mouse embryonic stem cells.
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影响因子：
21.3
作者：
Feng, Wenyi;Collingwood, David;Boeck, Max E;Fox, Lindsay A;Alvino, Gina M;Fangman, Walton L;Raghuraman, Mosur K;Brewer, Bonita J
通讯作者：
Brewer, Bonita J
影响因子：
64.5
作者：
Goldberg AD;Banaszynski LA;Noh KM;Lewis PW;Elsaesser SJ;Stadler S;Dewell S;Law M;Guo X;Li X;Wen D;Chapgier A;DeKelver RC;Miller JC;Lee YL;Boydston EA;Holmes MC;Gregory PD;Greally JM;Rafii S;Yang C;Scambler PJ;Garrick D;Gibbons RJ;Higgs DR;Cristea IM;Urnov FD;Zheng D;Allis CD
通讯作者：
Allis CD
影响因子：
10.5
作者：
Drane, Pascal;Ouararhni, Khalid;Hamiche, Ali
通讯作者：
Hamiche, Ali
影响因子：
15.9
作者：
Huh, Michael S.;O'Dea, Tina Price;Picketts, David J.
通讯作者：
Picketts, David J.
影响因子：
2.7
作者：
De La Fuente, R;Viveiros, MM;Eppig, JJ
通讯作者：
Eppig, JJ