Nateri Abdolrahman S, Riera-Sans Lluís, Da Costa Clive, Behrens Axel
Mammalian Genetics Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.
Science. 2004 Feb 27;303(5662):1374-8. doi: 10.1126/science.1092880. Epub 2004 Jan 22.
Jun N-terminal kinases (JNKs) are essential for neuronal microtubule assembly and apoptosis. Phosphorylation of the activating protein 1 (AP1) transcription factor c-Jun, at multiple sites within its transactivation domain, is required for JNK-induced neurotoxicity. We report that in neurons the stability of c-Jun is regulated by the E3 ligase SCF(Fbw7), which ubiquitinates phosphorylated c-Jun and facilitates c-Jun degradation. Fbw7 depletion resulted in accumulation of phosphorylated c-Jun, stimulation of AP1 activity, and neuronal apoptosis. SCF(Fbw7) therefore antagonizes the apoptotic c-Jun-dependent effector arm of JNK signaling, allowing neurons to tolerate potentially neurotoxic JNK activity.
JNK(Jun氨基末端激酶)对于神经元微管组装和凋亡至关重要。激活蛋白1(AP1)转录因子c-Jun在其反式激活结构域内的多个位点发生磷酸化,是JNK诱导神经毒性所必需的。我们报告,在神经元中,c-Jun的稳定性受E3连接酶SCF(Fbw7)调控,该连接酶使磷酸化的c-Jun泛素化并促进c-Jun降解。Fbw7缺失导致磷酸化c-Jun积累、AP1活性受刺激及神经元凋亡。因此,SCF(Fbw7)拮抗JNK信号通路中依赖c-Jun的凋亡效应臂,使神经元能够耐受潜在的神经毒性JNK活性。