Control of epithelial cell structure and developmental fate: lessons from Helicobacter pylori.
Control of epithelial cell structure and developmental fate: lessons from Helicobacter pylori.
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DOI：
10.1002/bies.20768
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发表时间：
2008-06
期刊：
影响因子：
--
通讯作者：
H. Mimuro;D. Berg;C. Sasakawa
中科院分区：
文献类型：
--
作者：
H. Mimuro;D. Berg;C. Sasakawa
通过研究细菌病原体如幽门螺杆菌与宿主组织的相互作用，可以对真核生物的调控回路产生有价值的见解。H.幽门螺杆菌使用IV型分泌系统（T4 SS）将其CagA毒力蛋白递送至上皮细胞，在上皮细胞中，大部分CagA毒力蛋白被磷酸化。CagA的磷酸化和非磷酸化形式各自与宿主调节蛋白相互作用以改变细胞结构和细胞命运。Kwok及其同事表明，CagA的磷酸化是通过宿主整合素作为受体和H。pylori的CagL蛋白作为整合素特异性粘附素，并且CagL-整合素结合激活负责CagA磷酸化的激酶级联。这项研究有助于理解传染病和细胞命运的控制。
Valuable insights into eukaryotic regulatory circuits can emerge from studying interactions of bacterial pathogens such as Helicobacter pylori with host tissues. H. pylori uses a type IV secretion system (T4SS) to deliver its CagA virulence protein to epithelial cells, where much of it becomes phosphorylated. CagA's phosphorylated and non-phosphorylated forms each interact with host regulatory proteins to alter cell structure and cell fate. Kwok and colleagues showed that CagA destined for phosphorylation is delivered using host integrin as receptor and H. pylori's CagL protein as an integrin-specific adhesin, and that CagL-integrin-binding activates the kinase cascade responsible for CagA phosphorylation. This research contributes to understanding infectious disease and the control of cell fates.