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AIM: To investigate whether cyclin-dependent kinase 5 and its regulatory protein p35 was involved in staurosporine-induced apoptosis of cortical neuronal cultures. METHODS: Primary cerebral cortical neurons were exposed to 300 nmol/L staurosporine. After incubation for different time, morphological alterations were observed with phase-contrast microscopy, fluorescence microscopy, and transmission electron microscopy. DNA fragmentation was detected by agarose gel electrophoresis. The protein levels of Cdk4, p53, Cdk5, and its regulatory protein p35 following staurosporine treatment were measured by Western blotting. The Cdk5 activity was assayed for histone H1 kinase activity by autoradiography. RESULTS: The typical morphological changes of apoptosis were observed and the nuclear DNA fragmentation showed the characteristic “ladder” pattern after the cells were treated by staurosporine. The Cdk5 protein level increased markedly at 3 h and continued to 24 h. The p35 level increased at 3 h after being expose
AIM: To investigate whether cyclin-dependent kinase 5 and its regulatory protein p35 was involved in staurosporine-induced apoptosis of cortical neuronal cultures. METHODS: Primary cerebral cortical neurons were exposed to 300 nmol / L staurosporine. After incubation for different time, morphological alterations were fragmented with phase-contrast microscopy, fluorescence microscopy, and transmission electron microscopy. The protein levels of Cdk4, p53, Cdk5, and its regulatory protein p35 following staurosporine treatment were measured by Western blotting. Cdk5 activity was assayed for histone H1 kinase activity by autoradiography. RESULTS: The typical morphological changes of apoptosis were observed and the nuclear DNA fragmentation showed the characteristic “ladder” pattern after the cells were treated by staurosporine. The Cdk5 protein level increased markedly at 3 h and continued to 24 h. The p35 level increased at 3 h after being expose