In in host counteractive pathogen infection, abate airframe is injured and preventing oneself immunity disease to happen, way of I interferon signal develops main function, because this lodges for the night inside main body,the generation of I interferon is maintained the immunity of moderate to react with ensuring by the mechanism adjusting control of careful. Extensive element is changed it is important to decorate the play in in virus infection revulsive IFN-I arises and fighting virus to affect action gets more research, but the research of adjusting control mechanism in infection of bacterium of cause of disease is opposite less, and IFN-I resists in host bacterium of different cause of disease affects medium action mechanism ambiguous also.
HECTD3 is to belong to HECT join of familial element of an E3 extensive is enzymatic, the research to this albumen is at present very few. The research of Chen Ce true early days confirms researcher of institute of animal of Kunming of the Chinese Academy of Sciences, HECTD3 is conveyed high in breast cancer, prostate cancer, stimulative tumour cell is right of the medicaments that change cure fight a gender, increased tumor cell survive (Li Et Al. Cell Death Dis, 2013; Li Et Al. Neoplasia, 2013) ; Built Hectd3 gene to knock except small mouse model. On this foundation, old plan fact and group of friend of neat dawn of Kunming animal place spread out collaboration, announced HECTD3 produces all in all effect in the congenital immunity reaction of host. Hectd3 gene blemish small rat enhanced host significantly to Francis bacili of bacterium, n/med tuberculosis is mixed the infection that bacterium of cause of disease duplicates inside the afterbirth such as bacterium of Li Si spy fights a gender, basically be to pass demarcate to travel inside the body of the bacterium inside afterbirth and diffuse. Its are immanent molecular mechanism can upright for HECTD3 guide TRAF3 K63 catenary gets together more the generation that floats element changes stimulative I interferon. Hectd3 gene is short of the huge bite cell that break to affect a condition to fell to reduce the gene with revulsive way of I interferon signal to convey significantly in Francis, restrain Francis thereby the bacterium transmission inside body and diffuse, hectd3 gene blemish small rat is shown fight infection ability apparently, research hints HECTD3 may become a new drone that fights infection as a result.
This research work is a problem with HECTD3 Mediates TRAF3 Polyubiquitination And Type I IFN Induction During Bacterial Infection, on June 19 online publish on international periodical Journal Of Clinical Investigation. What the Li Fubing of Kunming animal place, Li Yang, Liang Huichun and Xu Tao are an article is collective the first author, qi Xiaopeng and old plan fact are the joint newsletter writer of the article. The support that this job got plan of research and development of key of ministry of science and technology, Chinese Academy of Sciences and committee of national science foundation wait.
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Graph: HECTD3 interpose guides TRAF3 K63 catenary floats element is changed decorate bacterium of stimulative cause of disease to influence generation of revulsive Ⅰ interferon. A. Hectd3 gene is knocked except restrain F. Novicida is downstream to BMDM cell Ⅰ interferon and its signal access the revulsive expression of target gene; B. HECTD3 interpose guides TRAF3 K63 catenary floats element is changed decorate; C-E: F of resistance of Hectd3 gene blemish small rat. Novicida infection; F: Scientific hypothesis sketch map.
