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