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Swiprosin-1 Expression Is Up-Regulated through Protein Kinase $C-{\theta}$ and $NF-{\kappa}B$ Pathway in T Cells

  • Kim, Young-Dae (School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, Gwangju Institute of Science and Technology) ;
  • Kwon, Min-Sung (School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, Gwangju Institute of Science and Technology) ;
  • Na, Bo-Ra (School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, Gwangju Institute of Science and Technology) ;
  • Kim, Hye-Ran (School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, Gwangju Institute of Science and Technology) ;
  • Lee, Hyun-Su (School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, Gwangju Institute of Science and Technology) ;
  • Jun, Chang-Duk (School of Life Sciences, Immune Synapse Research Center and Cell Dynamics Research Center, Gwangju Institute of Science and Technology)
  • Received : 2013.01.21
  • Accepted : 2013.02.21
  • Published : 2013.04.30

Abstract

Swiprosin-1 exhibits the highest expression in $CD8^+$ T cells and immature B cells and has been proposed to play a role in lymphocyte biology through actin remodeling. However, regulation of swiprosin-1 gene expression is poorly understood. Here we report that swiprosin-1 is up-regulated in T cells by PKC pathway. Targeted inhibition of the specific protein kinase C (PKC) isotypes by siRNA revealed that $PKC-{\theta}$ is involved in the expression of swiprosin-1 in the human T cells. In contrast, down-regulation of swiprosin-1 by A23187 or ionomycin suggests that calcium-signaling plays a negative role. Interestingly, swiprosin-1 expression is only reduced by treatment with $NF-{\kappa}B$ inhibitors but not by NF-AT inhibitor, suggesting that the $NF-{\kappa}B$ pathway is critical for regulation of swiprosin-1 expression. Collectively, these results suggest that swiprosin-1 is a $PKC-{\theta}$-inducible gene and that it may modulate the late phase of T cell activation after antigen challenge.

Keywords

References

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