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Neuroligin-3-CSPG4 interaction maintains oligodendrocyte precursor cell progenitor state and promotes glioma proliferation through mechanotransduction
Glioma pathophysiology is robustly regulated by interactions with neurons. Key to these interactions is the role of neuroligin-3 (NLGN3), a synaptic adhesion molecule shed in response to neuronal activity that functions as a paracrine factor crucial for glioma growth. Here we elucidate the mechanist
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