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Cdk 5-mediated Phosphorylation of c-Myc on Ser-62 Is Essential in Transcriptional Activation of Cyclin B 1 by Cyclin G 1 *
| Content Provider | Semantic Scholar |
|---|---|
| Author | Seo, Haeng Ran Kim, Joon Bae, Sangwoo Soh, Jae-Won Lee, Yun-Sil |
| Copyright Year | 2008 |
| Abstract | It has been reported previously that cyclin G1 enables cells to overcome radiation-induced G2 arrest and increased cell death and that these effects aremediated by transcriptional activation of cyclin B1. In this study, we further investigated the mechanism by which cyclin G1 transcriptionally activates cyclin B1. Deletion or point mutations within the cyclin B1 promoter region revealed that the c-Myc binding site (E-box) is necessary for cyclinG1-mediated transcriptional activation of cyclin B1 to occur. In addition, the kinase activity of Cdk5 was increased by cyclin G1 overexpression, and Cdk5 directly phosphorylated c-Myc on Ser-62. Furthermore, cyclin G1 mediated increased radiosensitivity, and radiation-induced M phase arrest was attenuated when RNA interference of Cdk5 was treated. Taken together, the results of this study indicate that Cdk5 activation in cells that overexpress cyclin G1 leads to c-Myc phosphorylation on Ser-62, which is responsible for cyclin G1-mediated transcriptional activation of cyclin B1. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5c/5b/15601.PMC2414302.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
