Abstract:
: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.
journal_name
Immunityjournal_title
Immunityauthors
Tetsu O,Ishihara H,Kanno R,Kamiyasu M,Inoue H,Tokuhisa T,Taniguchi M,Kanno Mdoi
10.1016/s1074-7613(00)80627-5subject
Has Abstractpub_date
1998-10-01 00:00:00pages
439-48issue
4eissn
1074-7613issn
1097-4180pii
S1074-7613(00)80627-5journal_volume
9pub_type
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