Molecular mechanism of the abnormal expression of MHC-linked complement genes.

运用多种分子生物学技术，从分子水平研究了小鼠补体C4和Slp基因异常表达的调控机制。本研究得到了一些重要的发现，主要有以下几点：1 . H-2^k小鼠C4基因的低表达是由转录后和翻译前调控决定的。从肝脏cDNA文库中分离到C4 cDNA，其中含有可能由转剪接机制衍生的序列。在小鼠C4和Slp基因的5′区确定了转录调控结构域。识别方法与NF是同源的。kB/H2TF^1_在C4基因区域被鉴定，而在Slp基因区域未被鉴定。小鼠肝脏核因子与C4基因的这一识别位点结合，可能增强了C4基因的转录。

Regulatory mechanism underlying the abnormal expression of complement C4 and Slp genes of mouse was investigated at molecular level, using a wide variety of techniques of molecular biology. A few very important findings have been obtained from the present work which are summarized as follows.I.Post transckiptional and pretranslational regulation was shown to determine low C4 expression of C4 gene of H-2^k mouse(BlO.BR). C4 cDNA was isolated from the liver cDNA library which contains sequences probably derived by transsplicing mechanism.The transcriptional regulatory domains were identified in the 5' region of mouse C4 and Slp genes. The recognition mothif homologous to NF.kB/H2TF^1_ was identified in the region of C4 gene but not of Slp gene. Nuclear factors of mouse liver binds to this recognition mothif of C4 gene and probably enhance the transciption of C4 gene.