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|Title:||A novel CARD containing splice-isoform of CIITA regulates nitric oxide synthesis in dendritic cells||Authors:||Huang, D.
nitric oxide synthase
|Issue Date:||Mar-2010||Citation:||Huang, D., Lim, S., Chua, R.Y.R., Shi, H., Ng, M.L., Wong, S.H. (2010-03). A novel CARD containing splice-isoform of CIITA regulates nitric oxide synthesis in dendritic cells. Protein and Cell 1 (3) : 291-306. ScholarBank@NUS Repository. https://doi.org/10.1007/s13238-010-0039-5||Abstract:||MHC class II expression is controlled mainly at transcriptional level by class II transactivator (CIITA), which is a non-DNA binding coactivator and serves as a master control factor for MHC class II genes expression. Here, we describe the function of a novel splice-isoform of CIITA, DC-expressed caspase inhibitory isoform of CIITA (or DC-CASPIC), and we show that the expression of DCCASPIC in DC is upregulated upon lipopolysaccharides (LPS) induction. DC-CASPIC localizes to mitochondria, and protein-protein interaction study demonstrates that DC-CASPIC interacts with caspases and inhibits its activity in DC. Consistently, DC-CASPIC suppresses caspases-induced degradation of nitric oxide synthase-2 (NOS2) and subsequently promotes the synthesis of nitric oxide (NO). NO is an essential regulatory molecule that modulates the capability of DC in stimulating T cell proliferation/activation in vitro; hence, overexpression of DC-CASPIC in DC enhances this stimulation. Collectively, our findings reveal that DC-CASPIC is a key molecule that regulates caspases activity and NO synthesis in DC. © 2010 Higher Education Press and Springer-Verlag Berlin Heidelberg.||Source Title:||Protein and Cell||URI:||http://scholarbank.nus.edu.sg/handle/10635/108235||ISSN:||1674800X||DOI:||10.1007/s13238-010-0039-5|
|Appears in Collections:||Staff Publications|
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