Our further study also demonstrated that BRSK2 can interact directly with CDC25C and phosphorylate it at Ser216, sequestering it to cytoplasm.

• 我们的研究还发现BRSK2能够直接与CDC25C互作，并磷酸化CDC25C的Ser216位，从而将CDC25C滞留在细胞质中，这可能就是BRSK2引起细胞周期G2/M阻滞的分子机制。