The G2-M DNA damage checkpoint is an important cell cycle checkpoint in eukaryotic organisms that ensures that cells don't initiate mitosis until damaged or incompletely replicated DNA is sufficiently repaired.

G2/M DNA 损伤检查点可防止带有基因组 DNA 损伤的细胞进入有丝分裂（M 期）。特别指出的是，Cyclin B-cdc2 (CDK1) 复合体对调节 G2 转变非常重要，此时 cdc2 由酪氨酸激酶 Wee1 和 Myt1 维持在灭活状态。

2002年11月1日 · Defects in the G 2 -M arrest checkpoint may allow a damaged cell to enter mitosis and undergo apoptosis, and efforts to enhance this effect may increase the cytotoxicity of chemotherapy. Alternatively, efforts to increase G 2 -M arrest have also been associated with enhanced apoptosis.

There is increasing evidence that viral infection, expression of viral protein or the presence of viral DNA causes the host cell cycle to arrest during G2/M. The mechanisms used by viruses to cause arrest vary widely; some involve the activation of ...

2023年7月5日 · Increasing expression of P53, P21 and decreasing CCNB1, induction of cell G2/M cycle arrest, and consequently increase in the cell size can be suggested as one of the main mechanisms of...

Cdc2, the cyclin-dependent kinase that normally drives cells into mitosis, is an important target of pathways that mediate rapid arrest in G2 in response to DNA damage. Additional pathways ensure that the arrest is stably maintained.

2016年6月2日 · In the current study, we elucidated that erianin induced G2/M-phase arrest, apoptosis, and autophagy in human OS cells, which was mediated by ROS induction, leading to activation of JNK/c-Jun...

2001年4月5日 · Repression of the topoisomerase II gene by p53 helps to block entry into mitosis and strengthens the G2 arrest. In summary, multiple overlapping p53-dependent and p53-independent pathways...

2021年4月23日 · CDK1 plays key roles in cell cycle progression through the G2/M phase transition and activation of homologous recombination (HR) DNA repair pathway. Accordingly, various CDK1 inhibitors have been developed for cancer therapy that induce prolonged G2 arrest and/or sensitize cells to DNA damaging agents in tumor cells, resulting in cell death.

Vpr causes cell cycle G2/M arrest, but the triggering event occurs in the S phase of the cell cycle. Specifically we showed that the expression of HIV-1 vpr elicits activation of Chk1 through Ser 345 phosphorylation, which coincides with the hyperphosphorylation of Cdk1-Tyr 15, a …