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Checking in on hypoxia/reoxygenation.

机译：检查缺氧/复氧。

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摘要

Hypoxia/reoxygenation is a physiological stress that activates the DNA damage pathway. Significantly, this pathway is initiated during hypoxia, in the absence of detectable DNA damage. Our most recent study determined that during hypoxia, Chk 2 is phosphorylated in an ATM-dependent manner. In addition to this finding, we found that components of the MRN complex were not required for Chk 2 phosphorylation during hypoxia/reoxygenation. Once activated, Chk 2 initiates a signaling cascade, which induces a cell cycle arrest in the G2 phase. Loss of the Chk 2-mediated arrest correlated with an increase in sensitivity to hypoxia/reoxygenation. In contrast, loss of a p53-mediated reoxygenation-induced G1 arrest does not correlate with increased sensitivity to hypoxia/reoxygenation.
机译：缺氧/复氧是激活DNA损伤途径的生理应激。值得注意的是，该途径是在缺氧条件下启动的，没有可检测的DNA损伤。我们的最新研究确定，在缺氧期间，Chk 2会以ATM依赖性方式被磷酸化。除此发现外，我们发现缺氧/复氧过程中Chk 2磷酸化不需要MRN配合物的成分。一旦激活，Chk 2就会启动信号传导级联反应，从而在G2期诱导细胞周期停滞。 Chk 2介导的逮捕的丧失与对缺氧/复氧敏感性的增加有关。相比之下，p53介导的复氧诱导的G1阻滞的丧失与对缺氧/复氧的敏感性增加无关。

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