连合轴突的中线交叉和对Slit的反应性需要USP33。
Midline crossing and Slit responsiveness of commissural axons require USP33.
作者信息
Yuasa-Kawada Junichi, Kinoshita-Kawada Mariko, Wu Guan, Rao Yi, Wu Jane Y
机构信息
Department of Neurology, Lurie Comprehensive Cancer Center, Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
出版信息
Nat Neurosci. 2009 Sep;12(9):1087-9. doi: 10.1038/nn.2382. Epub 2009 Aug 16.
Commissural axons cross the ventral midline of the neural tube in a Slit-dependent manner. The underlying molecular mechanisms remain unclear. We found that the deubiquitinating enzyme USP33 interacts with the Robo1 receptor. USP33 was essential for midline crossing by commissural axons and for their response to Slit. Our results reveal a previously unknown role for USP33 in vertebrate commissural axon guidance and in Slit signaling.
连合轴突以依赖Slit的方式穿过神经管的腹侧中线。其潜在的分子机制仍不清楚。我们发现去泛素化酶USP33与Robo1受体相互作用。USP33对于连合轴突穿过中线及其对Slit的反应至关重要。我们的结果揭示了USP33在脊椎动物连合轴突导向和Slit信号传导中以前未知的作用。
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