Hu Qi-Dong, Ma Quan-Hong, Gennarini Gianfranco, Xiao Zhi-Cheng
Institute of Molecular and Cell Biology, Singapore General Hospital, Singapore, Singapore, and Department of Pharmacology and Human Physiology, University of Bari, Italy.
Dev Neurosci. 2006;28(1-2):25-33. doi: 10.1159/000090750.
Increasing evidence has shown that the Notch signalling pathway regulates oligodendrogliogenesis. Upon binding to classical Delta/Serrate/Lag-2 ligands, Notch signalling promotes generation of oligodendrocyte precursor cells while inhibiting their further differentiation into myelinating oligodendrocytes. In our recent studies, we have found that two neural cell adhesion molecules, F3/contactin and NB-3 interact with Notch receptors and promote oligodendrocyte development. Remarkably, all these F3 and NB-3/Notch cascade-related events required Deltex1 as the intermediate element. Experiments using several animal models further imply the function of F3/Notch signalling in vivo, which designates Notch signalling as a ligand-dependent, multipotential cascade involved in oligodendrocyte development.
越来越多的证据表明，Notch信号通路调节少突胶质细胞生成。在与经典的Delta/Serrate/Lag-2配体结合后，Notch信号通路促进少突胶质细胞前体细胞的生成，同时抑制它们进一步分化为髓鞘形成少突胶质细胞。在我们最近的研究中，我们发现两种神经细胞粘附分子F3/接触蛋白和NB-3与Notch受体相互作用并促进少突胶质细胞发育。值得注意的是，所有这些F3和NB-3/Notch级联相关事件都需要Deltex1作为中间元件。使用几种动物模型进行的实验进一步暗示了F3/Notch信号通路在体内的功能，这表明Notch信号通路是一种参与少突胶质细胞发育的依赖配体的多潜能级联反应。
