@article {Wang2018May,
	title = {Tissue and cellular rigidity and mechanosensitive signaling activation in Alexander disease},
	journal = {Nat. Commun.},
	volume = {9},
	number = {1},
	year = {2018},
	month = {May},
	pages = {1899},
	publisher = {Nature Publishing Group},
	abstract = {Glial cells have increasingly been implicated as active participants in the pathogenesis of neurological diseases, but critical pathways and mechanisms controlling glial function and secondary non-cell autonomous neuronal injury remain incompletely defined. Here we use models of Alexander disease, a severe brain disorder caused by gain-of-function mutations in GFAP, to demonstrate that misregulation of GFAP leads to activation of a mechanosensitive signaling cascade characterized by activation of the Hippo pathway and consequent increased expression of A-type lamin. Importantly, we use genetics to verify a functional role for dysregulated mechanotransduction signaling in promoting behavioral abnormalities and non-cell autonomous neurodegeneration. Further, we take cell biological and biophysical approaches to suggest that brain tissue stiffness is increased in Alexander disease. Our findings implicate altered mechanotransduction signaling as a key pathological cascade driving neuronal dysfunction and neurodegeneration in Alexander disease, and possibly also in other brain disorders characterized by gliosis.},
	issn = {2041-1723},
	doi = {10.1038/s41467-018-04269-7},
	url = {https://www.nature.com/articles/s41467-018-04269-7},
	author = {Wang, Liqun and Xia, Jing and Li, Jonathan and Hagemann, Tracy L. and Jones, Jeffrey R. and Fraenkel, Ernest and Weitz, DavidA. and Zhang, Su-Chun and Messing, Albee and Feany, Mel B.}
}
