CDK5 has been previously recognized mainly in the context of post-mitotic neurons; however, our findings reveal its critical role during mitosis. By specifically inhibiting CDK5 activity during this phase, significant mitotic defects, including nuclear atypia, were observed, indicating that CDK5 is essential for maintaining mitotic fidelity alongside CDK1.
Our experiments demonstrated that cyclin B1 acts as a mitotic co-factor to CDK5, forming a functional partnership that influences the overall process of mitosis. This complex between cyclin B1 and CDK5 not only reflects a novel interaction but emphasizes the need for both of these proteins to work together to ensure successful cell division.
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