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
作者： OlgaP Ryabinina , Ezhilkani Subbian , MihailS Iordanov
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摘要: The family of c-Jun NH2-terminal kinases (JNK) plays important roles in embryonic development and cellular responses to stress. Toxic metals their compounds are potent activators JNK mammalian cells. mechanism activation by cadmium sodium arsenite involves toxicant-induced oxidative study signaling pathways is complicated the significant degree redundancy among upstream regulators, especially at level kinase (JNKKK). Using Drosophila melanogaster S2 cells, we demonstrate here that activate (D-JNK) via stress as well, thus providing a simpler model system signaling. To elucidate lead D-JNK response or arsenite, employed RNA interference (RNAi) knock down thirteen regulators D-JNK, either singly combinations up seven time. D-MEKK1, fly orthologue MEKK4/MTK1, Hemipterous/D-MKK7 mediates arsenite.
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