p27Kip1: a key mediator of retinoic acid induced growth arrest in the SMS-KCNR human neuroblastoma cell line.

摘要: Retinoic acid (RA) treatment of SMS–KCNR neuroblastoma (NB) cells leads to G1 growth arrest and neuronal differentiation. To investigate the molecular mechanisms by which RA alters cell growth, we analysed expression activity components cycle machinery after culture in RA. Within 2 days prior NB phase cycle, there is a complete downregulation cyclin/Cdk activities. Protein levels for cyclin/Cdks were essentially unchanged during this time although was decrease steady-state p67N-Myc hyperphosphorylated Rb proteins. The Cdk inhibitors, p21Cip1 p27Kip1 constitutively expressed KCNR while p15INK4B p16INK4A not detected. induced an increase but p21Cip1. Furthermore, coincident with kinase bound p27Kip1. These results indicate that changes level its binding may play key role cells.