2005
DOI: 10.4161/cc.4.10.2055
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Inhibition of the ATR/Chk1 Pathway Induces a p38-Dependent S-phase Delay in Mouse ES Cells

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Cited by 27 publications
(28 citation statements)
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“…At 2 h, the distributions of the cells at different phases of the cell cycle were similar to that of control cells. However, there was an apparent accumulation of cells at the G2/M phase at 12 h, which become the majority of cell population of the cell cycle by 18 h. This is a pattern of G2/M arrest in ESCs similar to that caused by nocodazol [ 36 ]. After culture for 2 days, the cell cycle profi le signifi cantly recovered.…”
Section: Short-term Treatment Of Escs With H 2 O 2 Induced Transient mentioning
confidence: 76%
“…At 2 h, the distributions of the cells at different phases of the cell cycle were similar to that of control cells. However, there was an apparent accumulation of cells at the G2/M phase at 12 h, which become the majority of cell population of the cell cycle by 18 h. This is a pattern of G2/M arrest in ESCs similar to that caused by nocodazol [ 36 ]. After culture for 2 days, the cell cycle profi le signifi cantly recovered.…”
Section: Short-term Treatment Of Escs With H 2 O 2 Induced Transient mentioning
confidence: 76%
“…An important downstream target of ATR, Chk1, has been shown to modulate the S-phase checkpoint triggered by IR. In addition, inhibition of ATR function has recently been shown to result in the activation of p38 stress-activated protein kinase (Jirmanova et al, 2005), a cell cycle regulator. These diverse studies suggest that ATR might have multiple roles in the regulation of the cell cycle after IR treatment.…”
Section: Introductionmentioning
confidence: 99%
“…This has fostered the idea that progress through the terminal stage of G2 is guarded by an "antephase checkpoint" that works only during this period (Chin and Yeong 2010). This is a fallacy: In mammals, the p38 stress-activated checkpoint pathway functions throughout the cell cycle and can induce a delay or an arrest during G1 (e.g., Escote et al 2004;Lafarga et al 2009) or S (e.g., Jirmanova et al 2005), as well as anytime during G2. At the same time, there is no reason to suspect that the CHFR component of this pathway, which in normal cells is expressed at constant levels throughout the cell cycle (Burgess et al 2008), works only during antephase and not throughout all of G2 (or even G1) where one of its functions is to modify transcription activity through histone deacetylase 1 (Oh et al 2009).…”
Section: Entry Into Mitosis (The G2/m Transition)mentioning
confidence: 99%