Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression

Lamin B1 is a component of the nuclear lamina and plays a critical role in maintaining nuclear architecture, regulating gene expression and modulating chromatin positioning. We have previously shown that LMNB1 gene duplications cause autosomal dominant leukodystrophy (ADLD), a fatal adult onset demy...

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Veröffentlicht in:	The Journal of neuroscience 2015-08, Vol.35 (34), p.12002-12017
Hauptverfasser:	Rolyan, Harshvardhan, Tyurina, Yulia Y, Hernandez, Marylens, Amoscato, Andrew A, Sparvero, Louis J, Nmezi, Bruce C, Lu, Yue, Estécio, Marcos R H, Lin, Kevin, Chen, Junda, He, Rong-Rong, Gong, Pin, Rigatti, Lora H, Dupree, Jeffrey, Bayır, Hülya, Kagan, Valerian E, Casaccia, Patrizia, Padiath, Quasar S
Format:	Artikel
Sprache:	eng
Schlagworte:	Aging - genetics Aging - metabolism Animals Demyelinating Diseases - genetics Demyelinating Diseases - metabolism Gene Expression Regulation Humans Lamin Type B - biosynthesis Lipid Metabolism - physiology Mice Mice, Transgenic Nuclear Lamina - genetics Nuclear Lamina - metabolism Oligodendroglia - metabolism
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