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dc.contributor.authorXiong, Fuen_US
dc.contributor.authorXiao, Shaoboen_US
dc.contributor.authorYu, Meijuanen_US
dc.contributor.authorLi, Wanyien_US
dc.contributor.authorZheng, Huien_US
dc.contributor.authorShang, Yanchangen_US
dc.contributor.authorPeng, Funingen_US
dc.contributor.authorZhao, Cuipingen_US
dc.contributor.authorZhou, Wenliangen_US
dc.contributor.authorChen, Huanchunen_US
dc.contributor.authorFang, Liurongen_US
dc.contributor.authorChamberlain, Jeffrey S.en_US
dc.contributor.authorZhang, Chengen_US
dc.date.accessioned2010-04-21T15:48:38Z
dc.date.available2010-04-21T15:48:38Z
dc.date.issued2007en_US
dc.identifier.citationXiong F, Xiao S, Yu M, et al. Enhanced effect of microdystrophin gene transfection by HSV-VP22 mediated intercellular protein transport. BMC Neuroscience. 2007;8(1):50.en_US
dc.identifier.other10.1186/1471-2202-8-50en_US
dc.identifier.urihttp://www.biomedcentral.com/1471-2202/8/50en_US
dc.identifier.urihttp://hdl.handle.net/1773/15717
dc.description.abstractBackground: Duchenne musclar dystrophy (DMD) is an X-linked recessive disease caused by mutations of dystrophin gene, there is no effective treatment for this disorder at present. Plasmidmediated gene therapy is a promising therapeutical approach for the treatment of DMD. One of the major issues with plasmid-mediated gene therapy for DMD is poor transfection efficiency and distribution. The herpes simplex virus protein VP22 has the capacity to spread from a primary transduced cell to surrounding cells and improve the outcome of gene transfer. To improve the efficiency of plasmid-mediated gene therapy and investigate the utility of the intercellular trafficking properties of VP22-linked protein for the treatment for DMD, expression vectors for C-terminal versions of VP22-microdystrophin fusion protein was constructed and the VP22-mediated shuttle effect was evaluated both in vitro and in vivo. Results: Our results clearly demonstrate that the VP22-microdystrophin fusion protein could transport into C2C12 cells from 3T3 cells, moreover, the VP22-microdystrophin fusion protein enhanced greatly the amount of microdystrophin that accumulated following microdystrophin gene transfer in both transfected 3T3 cells and in the muscles of dystrophin-deficient (mdx) mice. Conclusion: These results highlight the efficiency of the VP22-mediated intercellular protein delivery for potential therapy of DMD and suggested that protein transduction may be a potential and versatile tool to enhance the effects of gene delivery for somatic gene therapy of DMD.en_US
dc.description.sponsorshipNational Natural Science Foundation of China (30370510, 30170337); CMB Fund (4209347); the Key Project of the State Ministry of Public Health (2001321); and National Nature Science Foundation of China (30400322).en_US
dc.language.isoen_USen_US
dc.titleEnhanced effect of microdystrophin gene transfection by HSV-VP22 mediated intercellular protein transporten_US
dc.typeArticleen_US


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