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Toll signaling promotes JNK-dependent apoptosis in Drosophila

机译:收费信号促进果蝇中的JNK依赖性细胞凋亡

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Apoptosis plays pivotal roles in organ development and tissue homeostasis, with its major function to remove unhealthy cells that may compromise the fitness of the organism. Toll signaling, with the ancient evolutionary origin, regulates embryonic dorsal–ventral patterning, axon targeting and degeneration, and innate immunity. Using Drosophila as a genetic model, we characterized the role of Toll signaling in apoptotic cell death. We found that gain of Toll signaling is able to trigger caspase-dependent cell death in development. In addition, JNK activity is required for Toll-induced cell death. Furthermore, ectopic Toll expression induces the activation of JNK pathway. Moreover, physiological activation of Toll signaling is sufficient to produce JNK-dependent cell death. Finally, Toll signaling activates JNK-mediated cell death through promoting ROS production. As Toll pathway has been evolutionarily conserved from Drosophila to human, this study may shed light on the mechanism of mammalian Toll-like receptors (TLRs) signaling in apoptotic cell death.
机译:细胞凋亡在器官发展和组织稳态中起着枢转作用,其主要功能去除可能损害生物体的适应性的不健康的细胞。随着古老的进化来源,调节胚胎背腹图案,轴突靶向和退化,以及先天免疫力。使用果蝇作为遗传模型,我们表征了Toll信号在凋亡细胞死亡中的作用。我们发现收费信令的增益能够在发育中触发依赖依赖的细胞死亡。此外,疾病诱导的细胞死亡需要JNK活动。此外,异位Toll表达诱导JNK途径的激活。此外,收费信号传导的生理活化足以产生JNK依赖性细胞死亡。最后,通过促进ROS生产来激活JNK介导的细胞死亡。随着收费途径从果蝇向人类流化,本研究可以在凋亡细胞死亡中的哺乳动物Toll样受体(TLRS)信号传导的机制上。

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