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G2-M regulators are essential for controlling the transition between the G2 phase and M phase of the cell cycle, ensuring proper cell division. This critical checkpoint allows the cell to repair DNA damage and prepare for mitosis, maintaining genomic stability.
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Activation of the G2/M checkpoint after DNA damage. In response to DNA damage, the ATM, ATR signaling pathway is activated, which leads to the phosphorylation and activation of Chk1 and Chk2 and to the subsequent phosphorylation of Cdc25. Phosphorylated Cdc25 is sequestered in the cytoplasm by 14-3-3 proteins, which prevents activation of cyclinB/Cdk1 by Cdc25 and results in G2 arrest. Activated ATM/ATR also activates p53-dependent signaling. This contributes to the maintenance of G2 arrest by upregulating 14-3-3, which sequesters Cdk1 in the cytoplasm. In addition, p53 induces the transactivation of p21, a Cdk inhibitor that binds to and inhibits cyclinB/Cdk1 complexes. P: phosphorylation.
The G2/M checkpoint is a crucial regulatory mechanism in the cell cycle that ensures cells do not enter mitosis with damaged or incompletely replicated DNA. Here are the key components involved in this regulation:
G2-M regulators play a crucial role in ensuring that cells do not enter mitosis with damaged DNA. At the G2-M checkpoint, cells assess DNA integrity and activate repair mechanisms if necessary. The G2-M transition is controlled by regulators like ATM/ATR and Chk1/Chk2 kinases, which respond to DNA damage by halting the cell cycle, allowing time for repair before mitosis begins.
The dysregulation of G2/M checkpoints is often observed in various cancers, making these regulators potential targets for therapeutic interventions. For instance:
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