Notch Receptor Activation Inhibits Oligodendrocyte Differentiation

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Notch Receptor Activation Inhibits Oligodendrocyte Differentiation

In this study, we show that oligodendrocyte differentiation is powerfully inhibited by activation of the Notch pathway. Oligodendrocytes and their precursors in the developing rat optic nerve express Notch1 receptors and, at the same time, retinal ganglion cells express Jagged1, a ligand of the Notch1 receptor, along their axons. Jagged1 expression is developmentally regulated, decreasing with ...

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Axoglial interaction via the notch receptor in oligodendrocyte differentiation.

INTRODUCTION Increasing evidence has revealed that the Notch signalling pathway is one of the pivotal systems that mediate oligodendrocyte development. The Notch receptor is a type I transmembrane molecule that represents a novel cellular signalling paradigm, namely, regulated intramembrane proteolysis (RIP). METHOD The typical Notch ligands, such as Delta, Serrate/Jagged and Lag2 (DSL), prom...

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Notch inhibits osteoblast differentiation and causes osteopenia.

Notch receptors are determinants of cell fate decisions. To define the role of Notch in the adult skeleton, we created transgenic mice overexpressing the Notch intracellular domain (NICD) under the control of the type I collagen promoter. First-generation transgenics were small and osteopenic. Bone histomorphometry revealed that NICD caused a decrease in bone volume, secondary to a reduction in...

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Extracellular Acidic pH Inhibits Oligodendrocyte Precursor Viability, Migration, and Differentiation

Axon remyelination in the central nervous system requires oligodendrocytes that produce myelin. Failure of this repair process is characteristic of neurodegeneration in demyelinating diseases such as multiple sclerosis, and it remains unclear how the lesion microenvironment contributes to decreased remyelination potential of oligodendrocytes. Here, we show that acidic extracellular pH, which is...

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ژورنال

عنوان ژورنال: Neuron

سال: 1998

ISSN: 0896-6273

DOI: 10.1016/s0896-6273(00)80515-2