Chunling Chen

发表

A Functional Null Mutation of SCN1B in a Patient with Dravet Syndrome

N. Nukina, P. de Jonghe, L. Claes, 2009, The Journal of Neuroscience.

Na+ Channel Scn1b Gene Regulates Dorsal Root Ganglion Nociceptor Excitability in Vivo*

W. Brackenbury, L. Isom, L. López-Santiago, 2011, The Journal of Biological Chemistry.

Channelopathy as a SUDEP Biomarker in Dravet Syndrome Patient-Derived Cardiac Myocytes

Vassilios J. Bezzerides, A. Goldman, J. Parent, 2018, Stem cell reports.

Sodium channel Scn1b null mice exhibit prolonged QT and RR intervals.

D. McEwen, J. Noebels, A. Lopatin, 2007, Journal of molecular and cellular cardiology.

Identification of the Cysteine Residue Responsible for Disulfide Linkage of Na+ Channel α and β2 Subunits*

J. Salzer, L. Isom, Chunling Chen, 2012, The Journal of Biological Chemistry.

The adhesion function of the sodium channel beta subunit (β1) contributes to cardiac action potential propagation

James W. Smyth, J. Gorelik, I. Deschênes, 2018, eLife.

Scn1b deletion in adult mice results in seizures and SUDEP

Sara J. Aton, Brittany C. Clawson, J. Parent, 2019, Annals of clinical and translational neurology.

Tyrosine-phosphorylated and Nonphosphorylated Sodium Channel β1 Subunits Are Differentially Localized in Cardiac Myocytes*

J. Malhotra, L. Isom, Chunling Chen, 2004, Journal of Biological Chemistry.

Floxed allele for conditional inactivation of the voltage‐gated sodium channel β1 subunit Scn1b

N. Nukina, L. Isom, Chunling Chen, 2007, Genesis.

Mapt deletion fails to rescue premature lethality in two models of sodium channel epilepsy

M. Meisler, J. Noebels, R. Bunton-Stasyshyn, 2018, Annals of clinical and translational neurology.

Reduced sodium channel density, altered voltage dependence of inactivation, and increased susceptibility to seizures in mice lacking sodium channel β2-subunits

William A Catterall, Angus M. Brown, Peter Shrager, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Antisense oligonucleotides increase Scn1a expression and reduce seizures and SUDEP incidence in a mouse model of Dravet syndrome

I. Aznarez, S. Leiser, L. Isom, 2020, Science Translational Medicine.

Regulation of Persistent Na Current by Interactions between β Subunits of Voltage-Gated Na Channels

Tina M. Grieco-Calub, I. Raman, L. Isom, 2009, The Journal of Neuroscience.

Open-Channel Block by the Cytoplasmic Tail of Sodium Channel β4 as a Mechanism for Resurgent Sodium Current

I. Raman, J. Malhotra, L. Isom, 2005, Neuron.

Sodium Channel β1 Subunit-mediated Modulation of Nav1.2 Currents and Cell Surface Density Is Dependent on Interactions with Contactin and Ankyrin*

D. McEwen, L. Isom, Chunling Chen, 2004, Journal of Biological Chemistry.

Cloning and expression of a zebrafish SCN1B ortholog and identification of a species-specific splice variant

L. Isom, E. Slat, Chunling Chen, 2007, BMC Genomics.

Sodium Channel β2 Subunits Regulate Tetrodotoxin-Sensitive Sodium Channels in Small Dorsal Root Ganglion Neurons and Modulate the Response to Pain

I. Decosterd, L. Isom, J. Wiley, 2006, The Journal of Neuroscience.

Functional reciprocity between Na+ channel Nav1.6 and β1 subunits in the coordinated regulation of excitability and neurite outgrowth

N. Nukina, W. Brackenbury, L. Isom, 2010, Proceedings of the National Academy of Sciences.

Characterization of Sodium Channel α- and β-Subunits in Rat and Mouse Cardiac Myocytes

R. Kass, I. Rivolta, J. Malhotra, 2001 .

Scn1b deletion leads to increased tetrodotoxin‐sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts

G. Fishman, J. Jalife, M. Delmar, 2015, The Journal of physiology.

Scn1b deletion leads to increased tetrodotoxin-sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts.

G. Fishman, J. Jalife, M. Delmar, 2014, The Journal of physiology.

Mice Lacking Sodium Channel β1 Subunits Display Defects in Neuronal Excitability, Sodium Channel Expression, and Nodal Architecture

Lori L. Isom, William A. Catterall, Peter Shrager, 2004, The Journal of Neuroscience.

Voltage-Gated Na+ Channel β1 Subunit-Mediated Neurite Outgrowth Requires Fyn Kinase and Contributes to Postnatal CNS Development In Vivo

W. Brackenbury, L. Isom, B. Ranscht, 2008, The Journal of Neuroscience.

Sodium Channel β1 Subunits Promote Neurite Outgrowth in Cerebellar Granule Neurons*

L. Isom, Chunling Chen, Tigwa H. Davis, 2004, Journal of Biological Chemistry.

Sodium channel beta1 subunits promote neurite outgrowth in cerebellar granule neurons.

L. Isom, Chunling Chen, Tigwa H. Davis, 2004, The Journal of biological chemistry.

Voltage-Gated Na+ Channel β1B: A Secreted Cell Adhesion Molecule Involved in Human Epilepsy

G. Rouleau, W. Brackenbury, R. Lafreniére, 2011, The Journal of Neuroscience.

Scn2b Deletion in Mice Results in Ventricular and Atrial Arrhythmias

J. Jalife, M. Delmar, J. Anumonwo, 2016, Circulation. Arrhythmia and electrophysiology.

The voltage-gated Na+ channel β3 subunit does not mediate trans homophilic cell adhesion or associate with the cell adhesion molecule contactin

D. McEwen, L. Isom, Chunling Chen, 2009, Neuroscience Letters.

Excitatory and inhibitory neuron defects in a mouse model of Scn1b‐linked EIEE52

Nicholas Denomme, J. M. Hull, Yukun Yuan, 2020, Annals of clinical and translational neurology.

Mapt deletion fails to rescue premature lethality in two models of sodium channel epilepsy

M. Meisler, J. Noebels, R. Bunton-Stasyshyn, 2018, Annals of clinical and translational neurology.

Identification of the Cysteine Residue Responsible for Disulfide Linkage of Na+ Channel α and β2 Subunits*

J. Salzer, L. Isom, Chunling Chen, 2012, The Journal of Biological Chemistry.