Yap and Taz regulate proliferation and differentiation of Schwann cells, driving radial sorting, myelination and myelin maintenance of peripheral nerves.
High PI3K-Akt-mTORC1 activity inhibits Schwann cell differentiation, while after onset of myelination, residual PI3K-Akt-mTORC1 activity promotes myelin growth.
Uncoupling the immunological response and degenerative processes from possible repair demonstrates that remyelination prevents axonal loss after inflammatory demyelination.
A combined approach of unbiased proteomics, biochemistry, genetics, and transgenic animal models reveals that GPR56/ADGRG1 regulates myelin formation and repair by interacting with its microglial-derived ligand transglutaminase 2.
A fully automated high-resolution in vivo screening platform for zebrafish was implemented and used to identify novel compounds that regulate oligodendrocyte lineage progression.
Electrically active axons in white matter stimulate their own myelination by releasing glutamate, which signals through AMPA-type glutamate receptors on nearby oligodendrocyte precursors and newly-differentiating oligodendrocytes, enhancing their survival and hence their ability to myelinate.
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.
Production of remyelinating subventricular zone oligodendrocyte progenitors is stimulated by transient abrogation of thyroid hormone signalling in the adult neural stem cell niche.
Mild myelin disruption leads to early axonal pathology, a novel pathological response in neural stem cells, regionally increased oligodendrocytes and altered behavior.
OPC-specific genetic inhibition of Akt upstream and downstream molecules in the mouse, and simultaneous OPC fate analysis reveal that PTEN-AKT-GSK3b forms a persistent negative signaling pathway for OL development, in parallel with the AKT-mTORC1 pathway.
