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細(xì)胞漿液是如何抵抗入侵細(xì)菌的?英國(guó)醫(yī)學(xué)研究委員會(huì)喊你來(lái)做博士生 已有2人參與
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單位：Medical Research Council (Cambridge), Laboratory of Molecular Biology 項(xiàng)目簡(jiǎn)介：The cytosol of mammalian cells should be an attractive niche for bacterial pathogens since it is rich in nutrients. However, most intracellular bacteria avoid the cytosol and rather live in vesicles. We think this paradox is caused by autophagy and other powerful, but poorly characterized, innate mechanisms that protect the cytosol (reviewed in Randow et al., Science 2013). Our lab has recently identified several genes that defend the cytosol against bacterial invasion: Galectin-8, a cytosolic lectin and novel danger receptor, catches bacteria by sensing the membrane damage caused during their entry into the cytosol (Thurston et al., Nature 2012). NDP52, besides acting in the Galectin-8 pathway, is also a receptor for bacteria that have become ubiquitin-coated, a poorly understood fate certain bacteria undergo when entering the cytosol (Thurston et al., Nature Immunol 2009). LC3C, yet anotherlig and of NDP52, is essential for a highly selective autophagy pathway that prevents bacteria from colonizing the cytosol (Muhlinen et al., Mol Cell 2012). Our discoveries have raised several new questions. For example, is Galectin-8 a danger receptor specific for bacteria or does it have further functions, for example in anti-viral immunity? Which E3 ubiquitin ligase coats cytosolic bacteria with ubiquitin? And maybe the most important question, how does this E3 recognize invading bacteria, i.e. is it a novel pattern recognition receptor? A position for an enthusiastic PhD student interested in cell-autonomous defence against bacteria or viruses is available. The project will employ a wide variety of molecular and immunological methods. 截止日期： 2015.12.02 聯(lián)系人： Dr F Randow （randow@mrc-lmb.cam.ac.uk） 詳細(xì)信息： http://mp.weixin.qq.com/s?__biz= ... becf5e62815a79fa#rd |
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