Unc119保护从志贺氏杆菌感染通过抑制Abl激酶家族。
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Vepachedu R,卡里姆Z,帕特尔啊,阿拉姆Goplen N, R
Unc119保护从志贺氏杆菌感染通过抑制Abl激酶家族。
《公共科学图书馆•综合》。2009;4 (4):e5211。doi: 10.1371 / journal.pone.0005211。Epub 2009年4月17日。
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19381274 (在PubMed]
- 文摘
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背景:细菌与细胞表面受体和细胞内信号分子进入细胞。Unc119适配器蛋白质,与受体酪氨酸激酶。它的角色在细菌入侵细胞是未知的。方法/主要结果:我们使用生化、分子和细胞生物学方法来识别Unc119的约束力的合作伙伴,和研究的影响Unc119 Abl激酶家族和志贺氏杆菌感染。我们使用功能丧失和gain-in-function方法研究的影响Unc119肺部志贺氏菌病的小鼠模型。Unc119与家庭Abl激酶相互作用,抑制激酶活性。因此,它能抑制Crk磷酸化,对志贺氏杆菌感染至关重要。Unc119硝唑Crk和志贺氏杆菌感染细胞。志贺氏杆菌传染性Unc119-deficient上皮细胞和巨噬细胞的增加。志贺氏菌病的小鼠模型cell-permeable TAT-Unc119抑制志贺氏杆菌感染。 Conversely, Unc119 knockdown in vivo results in enhanced bacterial invasion and increased lethality. Unc119 is an inducible protein. Its expression is upregulated by probacteria and bacterial products such as lipopolysacharide and sodium butyrate. The latter inhibits Shigella infection in mouse lungs but is ineffective in Unc119 deficiency. CONCLUSIONS: Unc119 inhibits signaling pathways that are used by Shigella to enter the cell. As a consequence it provides partial but significant protection from Shigella infections. Unc119 induction in vivo boosts host defense against infections.