CDK5 binds p25

p25 has a 5-10 fold longer half-life compared to p35 and lacks the membrane anchoring signal, which results in its constitutive activation and mislocalization of the CDK5:p25 complex to the cytoplasm and the nucleus (Patrick et al. 1999). As CDK5 deregulation triggers nuclear envelope dispersion (Chang et al. 2011), with timing being uncertain, all phosphorylation events catalyzed by the CDK5:p25 complex are shown to occur in the cytosol.

p25相较于p35具有5-10倍的更长半衰期，且缺乏膜锚定信号，这导致其构成性激活，以及CDK5:p25复合物在细胞质和细胞核中的错误定位（参见Patrick等人的研究，1999年）。由于CDK5的失调可引发核被膜扩散（Chang等人，2011年），其具体发生时机尚不明确，因此所有由CDK5:p25复合物催化的磷酸化事件均被证明发生在细胞质中。