Regular ArticleDystonin Expression in the Developing Nervous System Predominates in the Neurons That Degenerate indystonia musculorumMutant Mice
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Microtubule-Associated Proteins: Structuring the Cytoskeleton
2019, Trends in Cell BiologyFunctional and Genetic Analysis of Neuronal Isoforms of BPAG1
2016, Methods in EnzymologyCitation Excerpt :For the study of neuronal dystonin in primary cells, we recommend using sensory neurons derived from DRGs. This is due to the consistently high expression of the neuronal BPAG1 isoforms in sensory neurons (Bernier et al., 1995; Dowling, Yang, Wollmann, Reichardt, & Fuchs, 1997), as well as its major involvement in the dt disease. It also seems that BPAG1 loss-of-function in sensory neurons is not compensated for by other members of the spectraplakin family (Leung et al., 2001), which makes this cell type ideal for investigating the specific cellular roles of BPAG1 isoforms.
Cellular and Molecular Biology of Neuronal Dystonin
2013, International Review of Cell and Molecular BiologyCitation Excerpt :Dystonin-a is expressed in the spinal cord and brain at various embryonic and postnatal time points, including embryonic (E9.5–E16.5), postnatal (P3 and P42) and adult stages. Dystonin-a expression is highest at sexual maturity (P42) (Bernier et al., 1995). The presence of dystonin-a as early as E9.5 is interesting since the dt phenotype is only overtly obvious at approximately 2 weeks postnatal development.
Development of primary sensory neurons in the trigeminal nervous system; dependency on neurotrophins and other substances
2012, Japanese Dental Science ReviewAcetylcholinesterase activity in the brain of dystonia musculorum (Dst <sup>dt-J</sup>) mutant mice
2012, Neuroscience ResearchTargeted inactivation of a developmentally regulated neural plectin isoform (plectin 1c) in mice leads to reduced motor nerve conduction velocity
2009, Journal of Biological Chemistry