Regulation Of HSF1on Expression Of Dp71

Dp71is one of the most widely expressed isoforms of the dystrophin gene family.Its study in recent years displayed its important function of the nervous system:support the development and maintaining the normal physiological function of the nervous system. Also it plays an important role in the adhesion and proliferation process of the neuronal cells. As one of the most important transcriptional molecules in the heat shock process, heat shock factor1(HSF1) also participate in the transcriptional process of other molecules such as iNOS、 Fas other than heat shock proteins. It is found, there is one HSE in the promoter region of Dp71via bio-informatics software analysis, thus demonstrate the possibility that HSF1can regulate the expression of Dp71. In our project, we try to analysis the possibility on the regulation of HSF1on the expression of Dp71, which ultimate serves as possible explanation on the series neuronal symptoms of HSF1knock out mice.The following methods were employed in our project to explore our hypothesis:1.Western blot and real time RT-PCR were used to analysis the mRNA and protein expression in HSF1+/+and HSF-/-mice;2.PcDNA3.1-HSF1plasmids and Psilencer-HSF1plasmids were transected into A549cells, Western blot and real time RT-PCR were performed to analysis weather the change of expression of HFS1can influence the mRNA and protein expression of Dp71in A549cells;3EMSA and luciferase reporter system were employed to analysis the weather HSF1can bind the HSE in the Dp71promoter region.The following results were obtained in our project:1. The mRNA and protein expression of Dp71were reduced compared with HSF1+mice, the expression of the brain, lung, liver and kidney were statistically different.2. Over expression and expression deficiency of HSF1can significant influence the mRNA and protein expression of Dp71in A549cells.3EMSA and luciferase reporter system demonstrate that HSF1can bind the HSE in the promoter region of Dp71.(16pictures,2tables,56references)...