A TCF7L2-responsive suppression of both homeostatic and compensatory remyelination in Huntington disease mice
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Originalsprog | Engelsk |
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Artikelnummer | 111291 |
Tidsskrift | Cell Reports |
Vol/bind | 40 |
Udgave nummer | 9 |
Antal sider | 22 |
ISSN | 2211-1247 |
DOI | |
Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
Supported by the Hereditary Disease Foundation , NIH R01NS110776 , the Lundbeck Foundation , and Sana Biotechnology . We are grateful to both the URMC Genomics Research Center and the URMC Shared Resource Laboratory, for assistance with electron microscopy and mass spectrometry, respectively.
Funding Information:
Supported by the Hereditary Disease Foundation, NIH R01NS110776, the Lundbeck Foundation, and Sana Biotechnology. We are grateful to both the URMC Genomics Research Center and the URMC Shared Resource Laboratory, for assistance with electron microscopy and mass spectrometry, respectively. D.C.-M. prepared the OPCs used in the study; A.T. and R.S. performed the histological processing, imaging, and quantitative analyses; P.M.M. and A.B. generated the viral expression vectors used; K.M.C. performed the western blots of HD and WT white matter; L.C. performed the in vivo overexpression study and qPCRs; K.A.W. and J.N.M. were responsible for the mass spectrometry; K.B. was responsible for the electron microscopic imaging; J.N.M. performed the genomic analyses; A.B. and S.A.G. designed the study, analyzed data, and wrote the manuscript. S.A.G. is a part-time employee and stockholder of Sana Biotechnology, a cell therapy company, and his lab receives sponsored research support from Sana. S.A.G. is also a co-founder and adviser to CNS2 Therapeutics, another cell therapy company. None of the work described in this paper overlaps with his work with those companies. D.C.-M. is also a consultant to Sana.
Publisher Copyright:
© 2022 The Authors
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