Promyelocytic leukemia nuclear bodies behave as DNA damage sensors whose response to DNA double-strand breaks is regulated by NBS1 and the kinases ATM, Chk2, and ATR.
Promyelocytic leukemia nuclear bodies behave as DNA damage sensors whose response to DNA double-strand breaks is regulated by NBS1 and the kinases ATM, Chk2, and ATR.
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临时细胞性白血病核体的行为是DNA损伤传感器，其对DNA双链断裂的反应由NBS1和激酶ATM，CHK2和ATR调节。
DOI：
10.1083/jcb.200604009
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发表时间：
2006-10-09
期刊：
影响因子：
--
通讯作者：
Bazett-Jones DP
中科院分区：
文献类型：
--
作者：
Dellaire G;Ching RW;Ahmed K;Jalali F;Tse KC;Bristow RG;Bazett-Jones DP
早幼粒细胞白血病（PML）核体（NB）是一个动态的亚核区室，与肿瘤抑制以及DNA的转录、复制和修复有关。PML核体的数量在细胞周期中会发生变化，在S期以及对包括DNA损伤在内的细胞应激反应时会增加。尽管DNA损伤后染色质的拓扑结构变化可能会影响PML核体的完整性，但PML核体数量增加的分子或结构基础尚未阐明。我们证明，在DNA双链断裂诱导后，PML核体数量的增加是基于一个生物物理过程，以及持续的细胞周期进程和DNA修复。PML核体通过一种超分子裂变机制增加数量，该机制与在S期细胞中观察到的相似，并且会因NBS1、ATM、Chk2和ATR激酶功能缺失而延迟或受抑制。因此，PML核体数量的增加是细胞对DNA损伤反应的一个内在要素。
The promyelocytic leukemia (PML) nuclear body (NB) is a dynamic subnuclear compartment that is implicated in tumor suppression, as well as in the transcription, replication, and repair of DNA. PML NB number can change during the cell cycle, increasing in S phase and in response to cellular stress, including DNA damage. Although topological changes in chromatin after DNA damage may affect the integrity of PML NBs, the molecular or structural basis for an increase in PML NB number has not been elucidated. We demonstrate that after DNA double-strand break induction, the increase in PML NB number is based on a biophysical process, as well as ongoing cell cycle progression and DNA repair. PML NBs increase in number by a supramolecular fission mechanism similar to that observed in S-phase cells, and which is delayed or inhibited by the loss of function of NBS1, ATM, Chk2, and ATR kinase. Therefore, an increase in PML NB number is an intrinsic element of the cellular response to DNA damage.
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影响因子：
8
作者：
Carbone, R;Pearson, M;Pelicci, PG
通讯作者：
Pelicci, PG
影响因子：
7.3
作者：
Arienti, KL;Brunmark, A;Breitenbucher, JG
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Breitenbucher, JG
影响因子：
4.8
作者：
Eskiw, CH;Dellaire, G;Bazett-Jones, DP
通讯作者：
Bazett-Jones, DP
影响因子：
30.8
作者：
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通讯作者：
Meyn, MS
影响因子：
5.3
作者：
Buscemi, G;Savio, C;Delia, D
通讯作者：
Delia, D