| First Author | Tetsu O | Year | 1998 |
| Journal | Immunity | Volume | 9 |
| Issue | 4 | Pages | 439-48 |
| PubMed ID | 9806630 | Mgi Jnum | J:50623 |
| Mgi Id | MGI:1307018 | Doi | 10.1016/s1074-7613(00)80627-5 |
| Citation | Tetsu O, et al. (1998) mel-18 negatively regulates cell cycle progression upon B cell antigen receptor stimulation through a cascade leading to c-myc/cdc25. Immunity 9(4):439-48 |
| abstractText | mel-18 is a mammalian Polycomb group gene encoding a transcriptional repressor with tumor suppressive activity. Overexpression of mel-18 in mice results in cell cycle arrest of B cells upon B cell receptor stimulation with downregulation of c-myc. This phenotype is rescued in mel-18/c-myc double-transgenic mice, suggesting that c-myc locates downstream of mel-18. In mel-18 transgenic mice, the downregulation of cyclins D2 and E; CDK4, -6, and -7; and CDC25A causes the impairment in the activities of cyclin-dependent kinases, resulting in hypophosphorylation of the retinoblastoma protein. In contrast, the upregulation of c-Myc, CDC25, and CDC2/CDK2 kinase activities results in the augmentation of B cell proliferation in mel-18-deficient mice. We therefore propose that mel-18 negatively regulates the cell cycle through a c-myc/cdc25 cascade. |
