Fig. 9. Proposed model of G1/S cell cycle signaling controlled by CK2α in myoblasts. We observed delayed cell cycle progression through G1 phase supported by low levels of cyclin E and cyclin A in response to CK2α silencing. We additionally reported evidence of a marked increase in p27^KIP1 protein levels and inhibition of the cyclin E-CDK2 complex. p27^KIP1 inhibits the cyclin E-CDK2 complex which is one of the major upstream kinases of the retinoblastoma protein (Rb). This results in decreased phosphorylation of Rb at S795, which prevents subsequent release of E2F transcription factor bound to Rb. Increased phosphorylation at S10, and T197 of p27^KIP1 contribute to the up-regulation of this cyclin kinase inhibitor. The study presented here, additionally underlines the protective role of p27^KIP1 in myoblasts under growth conditions unfavorable for cell viability. Further details are discussed in the text.