CARD9 Mediates Dectin-2-induced IκBα Kinase Ubiquitination Leading to Activation of NF-κB in Response to Stimulation by the Hyphal Form of Candida albicans

作者: Liangkuan Bi , Sara Gojestani , Weihui Wu , Yen-Michael S. Hsu , Jiayuan Zhu

DOI: 10.1074/JBC.M110.131300

关键词:

摘要: The scaffold protein CARD9 plays an essential role in anti-fungus immunity and is implicated mediating Dectin-1/Syk-induced NF-κB activation response to Candida albicans infection. However, the molecular mechanism by which mediates C. albicans-induced not fully characterized. Here we demonstrate that involved induced hyphal form of hyphae (Hyphae) but its heat-inactivated unicellular form. Our data show inhibiting Dectin-2 expression selectively blocked Hyphae-induced NF-κB, whereas Dectin-1 mainly suppressed zymosan-induced indicating through Dectin-1. Consistently, find stimulation induces association with Bcl10, adaptor functions downstream also activation. This dependent on following stimulation. Finally, although both Syk are required for activation, they regulate different signaling events IκBα kinase ubiquitination, regulates phosphorylation. Together, our demonstrated Dectin-2-induced challenging.

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