Abstract
Abstractp21, a protein kinase inhibitor, was known to play a major role in the induction of G1 arrest in response to DNA damaging agent, but its role in G2/M transition was poorly understood. In this study, we investigated the involvement of p21 in mitomycin C‐induced G2 arrest in LP1‐1 cells. Treatment of mitomycin C at early G2 phase of LP1‐1 cells was found to induce G2 arrest and inhibit cdc2 kinase activity. However, expression of cyclin B and cdc2 protein were not affected by mitomycin C and an alteration of tyrosine dephosphorylation of cdc2 kinase could not be observed in the cells. On the other hand, p21 mRNA and protein were induced by mitomycin C. The binding of p21 protein to cyelin B‐cdc2 complex was increased and it was accompanied with the inactivation of cdc2 kinase after treatment of mitomycin C. These results suggest that mitomycin C‐induced G2 arrest may be mediated via increment of p21 level, elevation of binding ability with cyclin B‐cdc2 complex, and a subsequent reduction of cdc2 kinase activity.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
