Nitric Oxide Modulates the c-Jun N-terminal Kinase/Stress-Activated Protein Kinase Activity through Activating c-Jun N-Terminal Kinase Kinase

详细信息    查看全文

• 作者：Hanshin Kim ; Jaekyung Shim ; Pyung-Lim Han ; and Eui-Ju Choi
• 刊名：Biochemistry
• 出版年：1997
• 出版时间：November 4, 1997
• 年：1997
• 卷：36
• 期：44
• 页码：13677 - 13681
• 全文大小：184K
• 年卷期：v.36,no.44(November 4, 1997)
• ISSN：1520-4995

文摘

Nitric oxide is a signaling molecule that has a broadrange of physiological functions, includingneurotransmission, macrophage activation, and vasodilation. Themechanism by which nitric oxide regulatessignal transduction mediating diverse biological activities is notfully understood, however. Here, wedemonstrate that nitric oxide induced the stimulation of c-JunNH₂-terminal kinase (JNK)/stress-activatedprotein kinase (SAPK) in intact cells. Exposure of cultured HEK293cells to sodium nitroprusside, anitric oxide releasing agent, resulted in the stimulation of JNK1activity. The sodium nitroprusside-induced stimulation of JNK1 activity was abolished by treatment of cellswith N-acetylcysteine. Nitricoxide production from HEK293 cells ectopically expressing nitric oxidesynthases resulted in the stimulationof JNK1 activity, while JNK1 stimulation in nitric oxidesynthase-overexpressing cells was abrogated bya nitric oxide synthase inhibitor, N^G-nitro-L-arginine.Furthermore, exposure of cells to sodiumnitroprusside resulted in the stimulation of JNK kinase (JNKK1/SEK1).Taken together, our data suggestthat nitric oxide modulates the JNK activity through activatingJNKK1/SEK1.