Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination

By Corinna Lappe-Siefke, S. Goebbels, M. Gravel, E. Nicksch, John Lee, P. E. Braun, I. Griffiths, K. Nave. Nature Genetics, 2003

1,011 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/118339f7f96bd3d2491b6156af79e49522bfc8de

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Citations in the corpus

Oligodendrocytes: Myelination and Axonal Support. (2015, background): “2012), similar in phenotype to axonal degeneration caused by oligodendrocyte-specific defects (Griffiths et al. 1998; Lappe-Siefke et al. 2003).”
Neurotransmitter-Triggered Transfer of Exosomes Mediates Oligodendrocyte–Neuron Communication (2013, methodology): “Abbreviations: AAV, adeno-associated virus; AMPA, a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; CN, primary cortical neurons; CNP, 29, 39-cyclic nucleotide 39-phosphodiesterase; CNS, central nervous system; CSF, cerebrospinal fluid; div, days in vitro; GABA, c-aminobutyric acid; hrGFP, human”
Axon degeneration mechanisms: commonality amid diversity (2005, background): “fcgi?db=gene&cmd=Retrieve&dopt=full_report&list_uids=12799">CNP1 ) show numerous axonal swellings despite the presence of normal myeli”
High cholesterol level is essential for myelin membrane growth (2005, neutral): “To inactivate cholesterol biosynthesis in oligodendrocytes, we crossed SQS-flox mice with mice expressing Cre under the control of the 2′,3′-cyclic nucleotide phosphodiesterase (CNP) promoter (referred to as CNP-Cre mice”
Axon-glial signaling and the glial support of axon function. (2008, background): “Figure adapted from Lappe-Siefke et al. (2003).”
Remyelination in the CNS: from biology to therapy (2008, background): “Transgenic mice lacking the oligodendrocyte-expressed gene Cnp , which encodes a phosphodiesterase, or Plp , which encodes an integral myelin sheath protein, show long-term axonal degeneration, even in the presence of myelin sheaths that are either ultrastructurally normal or that show only mi”
The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. (2006, background): “Mice null for the glial cyclic nucleotide phosphodiesterase (Cnp1) gene developed axonal swellings and neurodegeneration throughout the brain, leading to hydrocephalus and premature death, but the ultrastructure, periodicity, and physical stability of myelin are apparently not altered (Lappe-Siefke ”