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M403461200v1
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Papers In Press, published online ahead of print June 8, 2004
J. Biol. Chem, 10.1074/jbc.M403461200
Submitted on March 29, 2004
Revised on June 2, 2004
Accepted on June 8, 2004

Nitric oxide inhibits glucocorticoid-induced apoptosis of thymocytes by repressing the SRG3 expression

Seung M. Jeong, Kyoo Y. Lee, Dongho Shin, Heekyoung Chung, Sung H. Jeon, and Rho H. Seong

Department of Biological Sciences, Seoul National University, Seoul, Seoul 151-742

Corresponding Author: rhseong{at}plaza.snu.ac.kr

Nitric Oxide (NO) plays many roles in the immune system. It has been known that NO rescued thymocytes from glucocorticoid (GC)-induced apoptosis. However, the downstream target of NO in the protection from GC-induced thymocyte apoptosis has yet to be identified. We previously reported that GC sensitivity of developing thymocytes is dependent on the expression level of SRG3. In this report, we found that NO repressed the SRG3 expression in both primary thymocytes and 16610D9 thymoma cells. Specifically, NO down-regulated the transcription of SRG3 via the inactivation of the transcription factor Sp1 DNA binding activity to the SRG3 promoter. In addition, overexpression of SRG3 by a heterologous promoter reduced NO-mediated rescue of thymocytes from GC-induced apoptosis. These observations strongly suggest that NO may be involved in protecting immature thymocytes from GC-induced apoptosis by repressing the SRG3 expression in thymus.


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