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Herbimycin A suppresses NF‐κB activation and tyrosine phosphorylation of JAK2 and the subsequent induction of nitric oxide synthase in C6 glioma cells
Author(s) -
Tadashi Nishiya,
Takashi Uehara,
Yasuyuki Nomura
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00933-z
Subject(s) - tyrosine phosphorylation , tyrosine kinase , nitric oxide synthase , phosphorylation , chemistry , tyrosine , tyrosine kinase inhibitor , lipopolysaccharide , nitric oxide , receptor tyrosine kinase , microbiology and biotechnology , cancer research , biology , biochemistry , signal transduction , endocrinology , organic chemistry , cancer , genetics
Herbimycin A, a potent tyrosine kinase inhibitor, suppressed nitric oxide synthase (NOS) induced by lipopolysaccharide (LPS) and interferon‐γ (IFN‐γ) in C6 glial cells. LPS activated NF‐κB, and this effect was inhibited by pretreatment with herbimycin A. In addition, IFN‐γ activated the tyrosine protein kinase, JAK2, and tyrosine‐phosphorylation by itself was also inhibited by herbimycin A. These results suggest that herbimycin A suppresses iNOS induction by inhibition of both NF‐κB activation caused by LPS, and tyrosine‐phosphorylation of JAK2 caused by IFN‐γ in C6 glioma cells.