D-MEKK1, the Drosophila orthologue of mammalian MEKK4/MTK1, and Hemipterous/D-MKK7 mediate the activation of D-JNK by cadmium and arsenite in Schneider cells |
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| Authors: | Olga P Ryabinina Ezhilkani Subbian Mihail S Iordanov |
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| Institution: | (1) Department of Cell and Developmental Biology, Oregon Health & Science University, Oregon, 97239, Portland;(2) Department of Biochemistry and Molecular Biology, Oregon Health & Science University, Oregon, 97239, Portland |
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| Abstract: | Background The family of c-Jun NH2-terminal kinases (JNK) plays important roles in embryonic development and in cellular responses to stress. Toxic metals and
their compounds are potent activators of JNK in mammalian cells. The mechanism of mammalian JNK activation by cadmium and
sodium arsenite involves toxicant-induced oxidative stress. The study of mammalian signaling pathways to JNK is complicated
by the significant degree of redundancy among upstream JNK regulators, especially at the level of JNK kinase kinases (JNKKK). |
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