Renegade nuclear enzymes disrupt axonal integrity.
Miller
Robert H
RH
The author is in the Department of Neurosciences, Case Western Reserve University, School of Medicine, Cleveland, Ohio, USA. rhm3@case.edu
D000818:Animals; D001370:Axonal Transport; D001369:Axons / Q000201:enzymology* / Q000502:physiology*; D002467:Cell Nucleus / Q000201:enzymology / Q000502:physiology; D003593:Cytoplasm / Q000201:enzymology / Q000276:immunology / Q000502:physiology; D003711:Demyelinating Diseases / Q000201:enzymology* / Q000276:immunology / Q000503:physiopathology; D056284:Histone Deacetylase 1 / Q000378:metabolism*; D006801:Humans; D051379:Mice; D008928:Mitochondria / Q000201:enzymology / Q000276:immunology / Q000502:physiology; D009103:Multiple Sclerosis / Q000201:enzymology / Q000276:immunology / Q000503:physiopathology; D009410:Nerve Degeneration / Q000201:enzymology* / Q000503:physiopathology
C110550:HDAC1 protein, human; C484389:Hdac1 protein, mouse; D056284:Histone Deacetylase 1