作者: Jing-Yuan Fang
关键词:
摘要: Cell cycle progression is regulated by interactions between cyclins and cyclin-dependent kinases (CDKs). p21(WAF1) one of the CIP/KIP family which inhibits CDKs activity. Increased expression may play an important role in growth arrest induced transformed cells. Although stability p21( WAF1) mRNA could be altered different signals, cell differentiation numerous influencing factors. However, recent studies suggest that two known mechanisms epigenesis, i.e.gene inactivation methylation promoter region changes to inactive chromatin histone deacetylation, seem best candidate for WAF1). To date, almost no coding mutations have been found tumor cells, despite extensive screening hundreds various tumors. Hypermethylation represent alternative mechanism p21(WAF1/CIP1) gene can inactivated. The reduction cellular DNMT protein levels also induces a corresponding rapid increase regulator demonstrating regulatory link independent DNA. Both hyperacetylation hypoacetylation appear carcinoma process, induction dietary fiber prevents carcinogenesis. Here, we review influence acetylation DNA on transcription, affection pathways or factors associated such as p 53, E2A, Sp1 well several deacetylation inhibitors.