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Cell cycle arrest at G2/M is a regulatory checkpoint that halts the cell cycle prior to mitosis, allowing cells time to repair DNA damage or incomplete replication before chromosome segregation[1][2][4]. The checkpoint is controlled by a network of kinases and phosphatases (ATM, ATR, Chk1, Chk2, p53, Cdc25, Wee1, etc.), acting primarily on the cyclin B1/CDK1 complex[1][2][3][4]. Dysregulation leads to genomic instability, unchecked cell division, and cancer. Some anticancer agents and DNA damaging drugs exploit this checkpoint to induce apoptosis in rapidly dividing cancer cells. However, the term "cell cycle arrest at G2/M" refers to a process and not to a distinct target molecule or receptor.

Other names

G2/M arrestG2-M DNA damage checkpointG2 phase cell cycle arrest

Induction of DNA damage to trigger checkpoint activation and halt progress at G2/M[1][3] - Inhibition or activation of checkpoint kinases (ATM, ATR, Chk1, Chk2) - Inhibition of Cdc25 phosphatases (block activation of CDK1/cyclin B1 complex, preventing entry to mitosis) - Disruption of CDK1/cyclin B1 complex and its regulators (Wee1, p21, p53)