作者: Mark K. Saville , Roger J. Watson
DOI: 10.1016/S0065-230X(08)60701-0
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摘要: Publisher Summary The chapter describes that B-Myb gene is subjected to two putative cyclin-dependent regulatory mechanisms during the cell cycle upregulation of mRNA abundance by derepression E2F/DRS-regulated transcription at G1/S boundary, and phosphorylation protein S phase. This dual mechanism has several features. First, it ensures in quiescent cells, there effectively no active because greatly down regulated little may be produced not activated kinases (Cdk)-mediated phosphorylation. Second, allows for a huge increase as cells go from G1 phase into Third, cycling partially inactivated dephosphorylation later stages only hyperactivated again on entry subsequent precise role B-myb regulation still unknown. transcriptional activator foreseen have function other genes whose products are involved synthesis components nucleotide biosynthesis DNA replication. As repressor, considered extinguishing expression negative regulators proliferation. BMyb potential activate promoters lack Myb binding site (MBS), these cannot predicted database searches. realization subject controls both its activity, this directs maximal activity phase, appears necessary proliferation leads conclude plays central downstream cyclins controlling basic coordinate passage through cycle.