相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。Positional stability of single double-strand breaks in mammalian cells
Evi Soutoglou et al.
NATURE CELL BIOLOGY (2007)
DNA methylation promotes Aurora-B-driven phosphorylation of histone H3 in chromosomal subdomains
Karine Monier et al.
JOURNAL OF CELL SCIENCE (2007)
Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks
S Bekker-Jensen et al.
JOURNAL OF CELL BIOLOGY (2006)
MDC1 maintains genomic stability by participating in the amplification of ATM-dependent DNA damage signals
ZK Lou et al.
MOLECULAR CELL (2006)
Dynamic assembly and sustained retention of 53BP1 at the sites of DNA damage are controlled by Mdc1/NFBD1
S Bekker-Jensen et al.
JOURNAL OF CELL BIOLOGY (2005)
Identification and characterization of a novel and specific inhibitor of the ataxia-telangiectasia mutated kinase ATM
I Hickson et al.
CANCER RESEARCH (2004)
Mdc1 couples DNA double-strand break recognition by Nbs1 with its H2AX-dependent chromatin retention
C Lukas et al.
EMBO JOURNAL (2004)
Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks
A Celeste et al.
NATURE CELL BIOLOGY (2003)
Chk1 and Chk2 kinases in checkpoint control and cancer
J Bartek et al.
CANCER CELL (2003)
NFBD1, like 53BP1, is an early and redundant transducer mediating Chk2 phosphorylation in response to DNA damage
AM Peng et al.
JOURNAL OF BIOLOGICAL CHEMISTRY (2003)
Distinct spatiotemporal dynamics of mammalian checkpoint regulators induced by DNA damage
C Lukas et al.
NATURE CELL BIOLOGY (2003)
MDC1 is required for the intra-S-phase DNA damage checkpoint
M Goldberg et al.
NATURE (2003)
MDC1 is a mediator of the mammalian DNA damage checkpoint
GS Stewart et al.
NATURE (2003)
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
CJ Bakkenist et al.
NATURE (2003)
DNA damage-induced G2-M checkpoint activation by histone H2AX and 53BP1
O Fernandez-Capetillo et al.
NATURE CELL BIOLOGY (2002)
ATM and ATR: networking cellular responses to DNA damage
Y Shiloh
CURRENT OPINION IN GENETICS & DEVELOPMENT (2001)