目的观察IGF2、H19在原发性肝癌中的表达并了解其意义。方法建立原发性肝癌模型,模型建立后第20周处死小鼠取肝癌及癌旁组织储存于-80℃备用,另取正常小鼠肝脏作对照,用Real time RT-PCR方法检测IGF2、H19 mRNA的变化。结果与对照组比较...目的观察IGF2、H19在原发性肝癌中的表达并了解其意义。方法建立原发性肝癌模型,模型建立后第20周处死小鼠取肝癌及癌旁组织储存于-80℃备用,另取正常小鼠肝脏作对照,用Real time RT-PCR方法检测IGF2、H19 mRNA的变化。结果与对照组比较,IGF2、H19在癌旁及癌组织中的表达都显著增加,在癌组织中增加更为显著P<0.05。结论 IGF2、H19的异常变化与小鼠原发性肝癌的发生发展有关。展开更多
Neural stem cells(NSCs) and imprinted genes play an important role in brain development. On historical grounds, these two determinants have been largely studied independently of each other. Recent evidence suggests, h...Neural stem cells(NSCs) and imprinted genes play an important role in brain development. On historical grounds, these two determinants have been largely studied independently of each other. Recent evidence suggests, however, that NSCs can reset select genomic imprints to prevent precocious depletion of the stem cell reservoir. Moreover, imprinted genes like the transcriptional regulator Zac1 can fine tune neuronal vs astroglial differentiation of NSCs. Zac1 binds in a sequence-specific manner to pro-neuronal and imprinted genes to confer transcriptional regulation and furthermore coregulates members of the p53-family in NSCs. At the genome scale, Zac1 is a central hub of an imprinted gene network comprising genes with animportant role for NSC quiescence, proliferation and differentiation. Overall, transcriptional, epigenomic, and genomic mechanisms seem to coordinate the functional relationships of NSCs and imprinted genes from development to maturation, and possibly aging.展开更多
文摘目的观察IGF2、H19在原发性肝癌中的表达并了解其意义。方法建立原发性肝癌模型,模型建立后第20周处死小鼠取肝癌及癌旁组织储存于-80℃备用,另取正常小鼠肝脏作对照,用Real time RT-PCR方法检测IGF2、H19 mRNA的变化。结果与对照组比较,IGF2、H19在癌旁及癌组织中的表达都显著增加,在癌组织中增加更为显著P<0.05。结论 IGF2、H19的异常变化与小鼠原发性肝癌的发生发展有关。
文摘Neural stem cells(NSCs) and imprinted genes play an important role in brain development. On historical grounds, these two determinants have been largely studied independently of each other. Recent evidence suggests, however, that NSCs can reset select genomic imprints to prevent precocious depletion of the stem cell reservoir. Moreover, imprinted genes like the transcriptional regulator Zac1 can fine tune neuronal vs astroglial differentiation of NSCs. Zac1 binds in a sequence-specific manner to pro-neuronal and imprinted genes to confer transcriptional regulation and furthermore coregulates members of the p53-family in NSCs. At the genome scale, Zac1 is a central hub of an imprinted gene network comprising genes with animportant role for NSC quiescence, proliferation and differentiation. Overall, transcriptional, epigenomic, and genomic mechanisms seem to coordinate the functional relationships of NSCs and imprinted genes from development to maturation, and possibly aging.
