Rbfox proteins regulate alternative splicing of neuronal sodium channel SCN8A

[1]  J. Jalife,et al.  A null mutation of the neuronal sodium channel NaV1.6 disrupts action potential propagation and excitation‐contraction coupling in the mouse heart , 2012, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[2]  Istvan Mody,et al.  The splicing regulator Rbfox1 (A2BP1) controls neuronal excitation in the mammalian brain , 2011, Nature Genetics.

[3]  J. Jalife,et al.  Abstract 12747: A Null Mutation of the Neuronal Sodium Channel Isoform Nav1.6 Disrupts Action Potential Propagation and EC Coupling in the Mouse Heart , 2010 .

[4]  Z. Nusser,et al.  Molecular Identity of Dendritic Voltage-Gated Sodium Channels , 2010, Science.

[5]  J. Manns,et al.  Dysfunction of the Scn8a Voltage-gated Sodium Channel Alters Sleep Architecture, Reduces Diurnal Corticosterone Levels, and Enhances Spatial Memory* , 2010, The Journal of Biological Chemistry.

[6]  D. Bergles,et al.  Excitability and Synaptic Communication within the Oligodendrocyte Lineage , 2010, The Journal of Neuroscience.

[7]  T. Tsukahara,et al.  Alternative splicing of Mef2c promoted by Fox‐1 during neural differentiation in P19 cells , 2010, Genes to cells : devoted to molecular & cellular mechanisms.

[8]  O. Mühlemann,et al.  Nonsense-mediated mRNA decay in human cells: mechanistic insights, functions beyond quality control and the double-life of NMD factors , 2010, Cellular and Molecular Life Sciences.

[9]  S. Kawamoto,et al.  Identification of Neuronal Nuclei (NeuN) as Fox-3, a New Member of the Fox-1 Gene Family of Splicing Factors* , 2009, The Journal of Biological Chemistry.

[10]  H. Kuroyanagi.  Fox-1 family of RNA-binding proteins , 2009, Cellular and Molecular Life Sciences.

[11]  D. Black,et al.  Developmental Control of CaV1.2 L-Type Calcium Channel Splicing by Fox Proteins , 2009, Molecular and Cellular Biology.

[12]  S. Remy,et al.  Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons. , 2008, Journal of neurophysiology.

[13]  D. Shao,et al.  Alternative splicing of Nav1.5: An electrophysiological comparison of ‘neonatal’ and ‘adult’ isoforms and critical involvement of a lysine residue , 2008, Journal of cellular physiology.

[14]  N. Kerr,et al.  Novel mRNA isoforms of the sodium channels Nav1.2, Nav1.3 and Nav1.7 encode predicted two-domain, truncated proteins , 2008, Neuroscience.

[15]  M. Meisler,et al.  Exaggerated emotional behavior in mice heterozygous null for the sodium channel Scn8a (Nav1.6) , 2008, Genes, brain, and behavior.

[16]  D. Attwell,et al.  Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter , 2008, Nature Neuroscience.

[17]  Y. Xing,et al.  A Transcriptome Database for Astrocytes, Neurons, and Oligodendrocytes: A New Resource for Understanding Brain Development and Function , 2008, The Journal of Neuroscience.

[18]  D James Surmeier,et al.  Nav1.6 Sodium Channels Are Critical to Pacemaking and Fast Spiking in Globus Pallidus Neurons , 2007, The Journal of Neuroscience.

[19]  Douglas L. Black,et al.  Neuronal regulation of alternative pre-mRNA splicing , 2007, Nature Reviews Neuroscience.

[20]  D. McEwen,et al.  Sodium channel Scn1b null mice exhibit prolonged QT and RR intervals. , 2007, Journal of molecular and cellular cardiology.

[21]  M. Meisler,et al.  Evidence for a direct role of the disease modifier SCNM1 in splicing. , 2007, Human molecular genetics.

[22]  Christa Lese Martin,et al.  Cytogenetic and molecular characterization of A2BP1/FOX1 as a candidate gene for autism , 2007, American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.

[23]  S. H. Chandler,et al.  Sodium currents in mesencephalic trigeminal neurons from Nav1.6 null mice. , 2007, Journal of neurophysiology.

[24]  Kenny Q. Ye,et al.  Strong Association of De Novo Copy Number Mutations with Autism , 2007, Science.

[25]  S. Brenner,et al.  Unproductive splicing of SR genes associated with highly conserved and ultraconserved DNA elements , 2007, Nature.

[26]  A. Ma,et al.  Downregulation of neuronal sodium channel subunits Nav1.1 and Nav1.6 in the sinoatrial node from volume-overloaded heart failure rat , 2007, Pflügers Archiv - European Journal of Physiology.

[27]  T. Speed,et al.  Functional Genomic Analysis of Oligodendrocyte Differentiation , 2006, The Journal of Neuroscience.

[28]  S. I. Levin,et al.  Impaired motor function in mice with cell-specific knockout of sodium channel Scn8a (NaV1.6) in cerebellar purkinje neurons and granule cells. , 2006, Journal of neurophysiology.

[29]  G. Matthews,et al.  Impaired Firing and Cell-Specific Compensation in Neurons Lacking Nav1.6 Sodium Channels , 2006, The Journal of Neuroscience.

[30]  C. Chabbert,et al.  Molecular diversity of voltage-gated sodium channel alpha subunits expressed in neuronal and non-neuronal excitable cells , 2005, Neuroscience.

[31]  Peter Stoilov,et al.  Homologues of the Caenorhabditis elegans Fox-1 Protein Are Neuronal Splicing Regulators in Mammals , 2005, Molecular and Cellular Biology.

[32]  M. Meisler,et al.  Heterozygosity for a protein truncation mutation of sodium channel SCN8A in a patient with cerebellar atrophy, ataxia, and mental retardation , 2005, Journal of Medical Genetics.

[33]  M. Meisler,et al.  Sodium channel mutations in epilepsy and other neurological disorders. , 2005, Journal of Clinical Investigation.

[34]  P. Silver,et al.  A genome-wide in situ hybridization map of RNA-binding proteins reveals anatomically restricted expression in the developing mouse brain , 2005, BMC Developmental Biology.

[35]  S. Dib-Hajj,et al.  Nav1.6 channels generate resurgent sodium currents in spinal sensory neurons , 2005, FEBS letters.

[36]  M. Meisler,et al.  Multiple transcripts of sodium channel SCN8A (Na(V)1.6) with alternative 5'- and 3'-untranslated regions and initial characterization of the SCN8A promoter. , 2005, Genomics.

[37]  M. Meisler,et al.  Allelic mutations of the sodium channel SCN8A reveal multiple cellular and physiological functions , 2004, Genetica.

[38]  J. Mulley,et al.  The de novo chromosome 16 translocations of two patients with abnormal phenotypes (mental retardation and epilepsy) disrupt the A2BP1 gene , 2004, Journal of Human Genetics.

[39]  B. Bean,et al.  Sodium currents in subthalamic nucleus neurons from Nav1.6-null mice. , 2004, Journal of neurophysiology.

[40]  W. Catterall,et al.  Distinct Subcellular Localization of Different Sodium Channel &agr; and &bgr; Subunits in Single Ventricular Myocytes From Mouse Heart , 2004, Circulation.

[41]  M. Meisler,et al.  SCNM1, a Putative RNA Splicing Factor That Modifies Disease Severity in Mice , 2003, Science.

[42]  L. Weiss,et al.  Sodium channels SCN1A, SCN2A and SCN3A in familial autism , 2003, Molecular Psychiatry.

[43]  S. Waxman,et al.  Sodium channel Na(v)1.6 is expressed along nonmyelinated axons and it contributes to conduction. , 2002, Brain research. Molecular brain research.

[44]  C. Steinhäuser,et al.  Glial membrane channels and receptors in epilepsy: impact for generation and spread of seizure activity. , 2002, European journal of pharmacology.

[45]  A. L. Goldin,et al.  Alternative Splicing of an Insect Sodium Channel Gene Generates Pharmacologically Distinct Sodium Channels , 2002, The Journal of Neuroscience.

[46]  G. Alcaraz,et al.  Molecular determinants of emerging excitability in rat embryonic motoneurons , 2002, The Journal of physiology.

[47]  Ben A. Barres,et al.  Retinal Ganglion Cells Do Not Extend Axons by Default Promotion by Neurotrophic Signaling and Electrical Activity , 2002, Neuron.

[48]  D. Surmeier,et al.  D1/D5 Dopamine Receptor Activation Differentially Modulates Rapidly Inactivating and Persistent Sodium Currents in Prefrontal Cortex Pyramidal Neurons , 2001, The Journal of Neuroscience.

[49]  A. Lieberman,et al.  Androgens regulate the mammalian homologues of invertebrate sex determination genes tra-2 and fox-1. , 2001, Biochemical and biophysical research communications.

[50]  S. Pulst,et al.  A novel protein with RNA-binding motifs interacts with ataxin-2. , 2000, Human molecular genetics.

[51]  J. Caldwell,et al.  Developmental and regional expression of sodium channel isoform NaCh6 in the rat central nervous system , 2000, The Journal of comparative neurology.

[52]  M. Meisler,et al.  Evolution and diversity of mammalian sodium channel genes. , 1999, Genomics.

[53]  S. Waxman,et al.  Novel splice variants of the voltage‐sensitive sodium channel alpha subunit , 1998, Neuroreport.

[54]  D L Black,et al.  A complex intronic splicing enhancer from the c-src pre-mRNA activates inclusion of a heterologous exon , 1997, Molecular and cellular biology.

[55]  I. Raman,et al.  Altered Subthreshold Sodium Currents and Disrupted Firing Patterns in Purkinje Neurons of Scn8a Mutant Mice , 1997, Neuron.

[56]  M. Meisler,et al.  Alternative Splicing of the Sodium Channel SCN8A Predicts a Truncated Two-domain Protein in Fetal Brain and Non-neuronal Cells* , 1997, Journal of Biological Chemistry.

[57]  W. Richardson,et al.  Cell death and control of cell survival in the oligodendrocyte lineage , 1992, Cell.

[58]  D. Corey,et al.  Ion channel expression by white matter glia: The type-1 astrocyte , 1990, Neuron.

[59]  F. Conti,et al.  Structural parts involved in activation and inactivation of the sodium channel , 1989, Nature.

[60]  David P. Corey,et al.  Immunological, morphological, and electrophysiological variation among retinal ganglion cells purified by panning , 1988, Neuron.

[61]  K. McCarthy,et al.  Preparation of separate astroglial and oligodendroglial cell cultures from rat cerebral tissue , 1980, The Journal of cell biology.

[62]  J. Williams,et al.  Origin of transmembrane potentials in non-excitable cells. , 1970, Journal of theoretical biology.