Aeromonas salmonicida-secreted protein AopP is a potent inducer of apoptosis in a mammalian and a Drosophila model.
Aeromonas salmonicida-secreted protein AopP is a potent inducer of apoptosis in a mammalian and a Drosophila model.
复制标题
DOI：
10.1111/j.1462-5822.2011.01717.x
复制
发表时间：
2012-02
影响因子：
3.4
通讯作者：
Moberg KH
中科院分区：
文献类型：
--
作者：
Jones RM;Luo L;Moberg KH
Some pathogens are able to establish themselves within the host because they have evolved mechanisms to disrupt host innate immunity. For example, a number of pathogens secrete preformed effector proteins via type III secretion apparati that influence innate immune or apoptotic signaling pathways. One group of effector proteins that usurp innate immune signaling is the YopJ-like family of bacterial effector proteins, which includes AopP from Aeromonas salmonicida. Aeromonas species are known to cause gastrointestinal disease in humans, and are associated mainly with subcutaneous wound infections and septicemia in other metazoans, particularly fish. AopP has been reported to have inhibitory activity against the NF-κB pathway in cultured cells, although the pathological outcomes of AopP activity have not been examined. Here, we show that AopP has potent pro-apoptotic activity when expressed in cultured mammalian macrophage or epithelial cells, or when ectopically expressed in Drosophila melanogaster hemocytes or imaginal disk epithelial cells. Furthermore, apoptosis was significantly elevated upon concurrent AopP expression and TNF-α cellular stimulation. Together, our results demonstrate how the specificity of a YopJ-like protein toward signaling pathways directly governs cellular pathological outcome in disease.
登录
查看更多内容
影响因子：
4.4
作者：
Collier-Hyams, LS;Zeng, H;Neish, AS
通讯作者：
Neish, AS
DOI：
10.1073/pnas.0510748103
发表时间：
2006-02-28
影响因子：
11.1
作者：
Guichard, A;Park, JM;Bier, E
通讯作者：
Bier, E
影响因子：
3
作者：
GLUSKIN, I;BATASH, D;BOLDUR, I
通讯作者：
BOLDUR, I
影响因子：
4.6
作者：
Kumar, JP;Hsiung, F;Moses, K
通讯作者：
Moses, K
影响因子：
11.4
作者：
Igaki, T;Kanda, H;Miura, M
通讯作者：
Miura, M