Ashwin Woodhoo

TL;DR: It is concluded that a single glial transcription factor is essential for restoration of damaged nerves, acting to control the transdifferentiation of myelin and Remak Schwann cells to dedicated repair cells in damaged tissue.

TL;DR: negative regulation of c-Jun is likely to have significant implications for three areas of Schwann cell biology: the molecular analysis of plasticity, demyelinating pathologies, and the response of peripheral nerves to injury.

TL;DR: It is demonstrated that activation of an inducible Raf-kinase transgene in myelinated Schwann cells is sufficient to control this plasticity by inducing severe demyelination in the absence of axonal damage, with the period of demYelination/ataxia determined by the duration of Raf activation.

TL;DR: Schwann cells degrade myelin after injury by a novel form of selective autophagy, myelinophagy which is positively regulated by the JNK/c-Jun pathway and is defective in the injured central nervous system.

TL;DR: Using transgenic mice and cell cultures, it is found that Notch has complex and extensive regulatory functions in Schwann cells, and this finding identifies a signaling pathway that induces myelin breakdown in vivo.