In vivo experiments on transgenic mice, and cell culture studies, establish Schwann cell c-Jun as a central regulator of peripheral nerve repair, and repair failure, during aging and chronic denervation.

The discovery of markers specific to perisynaptic Schwann cells will accelerate the discovery of mechanisms important for their differentiation and function.

Cd59 and developmental inflammation are key players in myelinating glial cell development, highlighting the collaboration between glia and the innate immune system to ensure normal neural development.

Schwann cell induced quiescence of mechanosensory progenitor cells is mediated by inhibition of Wnt/β-catenin signaling.

Angiogenesis and vascular development within peripheral nerve is regulated by Netrin-1, Schwann cells, and myelination.

In the peripheral nervous system, the large GTPase dynamin 2 is required for Schwann cell survival, developmental radial sorting of axons, myelination, and myelin maintenance.

Yap and Taz regulate proliferation and differentiation of Schwann cells, driving radial sorting, myelination and myelin maintenance of peripheral nerves.

YAP and TAZ, potent concoproteins and therapeutic targets in cancer therapy, are essential for Schwann cells to support peripheral nerve regeneration.

In a mouse model of neurofibromatosis type 1, the purinergic receptor P2RY14 is a key regulator of Schwann cell precursor self-renewal and proliferation, of neurofibroma tumor initiation and of mouse survival.

mTORC1 and c-Jun are implicated in a possible mechanism causing myelin loss downstream of mitochondrial dysfunction in Schwann cells.