Copper is essential for cyclin B1-mediated CDK1 activation

Jiaru Wang, Dian Yang, Hai-Fan Yu, Jing Jin, Yuzhe Nie, Sihua Zhang, Weiwei Ren, Zihan Ge, Zhuo Zhang, Xinghong Ma, Shaojun Dai, Guangchao Sui and Chun-Bo Teng ()
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Jiaru Wang: Northeast Forestry University
Dian Yang: Northeast Forestry University
Hai-Fan Yu: Northeast Forestry University
Jing Jin: Northeast Forestry University
Yuzhe Nie: Northeast Forestry University
Sihua Zhang: Northeast Forestry University
Weiwei Ren: Shanghai Normal University
Zihan Ge: Northeast Forestry University
Zhuo Zhang: Northeast Forestry University
Xinghong Ma: Northeast Agricultural University
Shaojun Dai: Shanghai Normal University
Guangchao Sui: Northeast Forestry University
Chun-Bo Teng: Northeast Forestry University

Nature Communications, 2025, vol. 16, issue 1, 1-12

Abstract: Abstract Cyclin-dependent kinase 1 (CDK1) is the pivotal kinase responsible for initiating cell division. Its activation is dependent on binding to regulatory cyclins, such as CCNB1. Our research demonstrates that copper binding to both CDK1 and CCNB1 is essential for activating CDK1 in cells. Mutations in the copper-binding amino acids of either CDK1 or CCNB1 do not disrupt their interaction but are unable to activate CDK1. We also reveal that CCNB1 facilitates the transfer of copper from ATOX1 to CDK1, consequently activating its kinase function. Disruption of copper transfer through the ATOX1-CCNB1-CDK1 pathway can impede CDK1 activation and halt cell cycle progression. In summary, our findings elucidate a mechanism through which copper promotes CDK1 activation and the G2/M transition in the cell cycle. These results could provide insight into the acquisition of proliferative properties associated with increased copper levels in cancer and offer targets for cancer therapy.

Date: 2025
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DOI: 10.1038/s41467-025-57538-7

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