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Publications by Fiona E. Holmes

Novel Isoforms of the Sodium Channels Nav1.8 and Nav1.5 Are Produced by a Conserved Mechanism in Mouse and Rat

Journal of Biological Chemistry

English

The Sodium Channel Nav1.5a Is the Predominant Isoform Expressed in Adult Mouse Dorsal Root Ganglia and Exhibits Distinct Inactivation Properties From the Full-Length Nav1.5 Channel

Molecular and Cellular Neurosciences

Molecular Neuroscience

English

Related publications

Sodium Channel Diversity in the Vestibular Ganglion: NaV1.5, NaV1.8, and Tetrodotoxin-Sensitive Currents

Journal of Neurophysiology

Neuroscience

Physiology

2016

English

Ca2+-Dependent Regulation of Sodium Channels NaV1.4 and NaV1.5 Is Controlled by the Post-Iq Motif

Nature Communications

English

Hypoxia Produces Pro-Arrhythmic Late Sodium Current in Cardiac Myocytes by SUMOylation of NaV1.5 Channels

English

Protein Kinase D Isoforms Are Expressed in Rat and Mouse Primary Sensory Neurons and Are Activated by Agonists of Protease-Activated Receptor 2

Journal of Comparative Neurology

Neuroscience

2009

English

Influence of Androgenic Blockade With Flutamide on Pain Behaviour and Expression of the Genes That Encode the NaV1.7 and NaV1.8 Voltage-Dependent Sodium Channels in a Rat Model of Postoperative Pain

Journal of Translational Medicine

English

Electrophysiological Properties of Mouse and Epitope-Tagged Human Cardiac Sodium Channel Nav1.5 Expressed in HEK293 Cells

English

Electrophysiological Properties of Mouse and Epitope-Tagged Human Cardiac Sodium Channel Nav1.5 Expressed in HEK293 Cells

English

A Subset of GAF Domains Are Evolutionarily Conserved Sodium Sensors

Molecular Microbiology

Microbiology

Molecular Biology

2007

English

Potent Inactivation-Dependent Inhibition of Adult and Neonatal NaV1.5 Channels by Lidocaine and Levobupivacaine

Anesthesia and Analgesia

Anesthesiology

Pain Medicine

2018

English

Amanote Research

Discover open access scientific publications

Search, annotate, share and cite publications

Publications by Fiona E. Holmes

Novel Isoforms of the Sodium Channels Nav1.8 and Nav1.5 Are Produced by a Conserved Mechanism in Mouse and Rat

The Sodium Channel Nav1.5a Is the Predominant Isoform Expressed in Adult Mouse Dorsal Root Ganglia and Exhibits Distinct Inactivation Properties From the Full-Length Nav1.5 Channel

Related publications

Sodium Channel Diversity in the Vestibular Ganglion: NaV1.5, NaV1.8, and Tetrodotoxin-Sensitive Currents

Ca2+-Dependent Regulation of Sodium Channels NaV1.4 and NaV1.5 Is Controlled by the Post-Iq Motif

Hypoxia Produces Pro-Arrhythmic Late Sodium Current in Cardiac Myocytes by SUMOylation of NaV1.5 Channels

Protein Kinase D Isoforms Are Expressed in Rat and Mouse Primary Sensory Neurons and Are Activated by Agonists of Protease-Activated Receptor 2

Influence of Androgenic Blockade With Flutamide on Pain Behaviour and Expression of the Genes That Encode the NaV1.7 and NaV1.8 Voltage-Dependent Sodium Channels in a Rat Model of Postoperative Pain

Electrophysiological Properties of Mouse and Epitope-Tagged Human Cardiac Sodium Channel Nav1.5 Expressed in HEK293 Cells

Electrophysiological Properties of Mouse and Epitope-Tagged Human Cardiac Sodium Channel Nav1.5 Expressed in HEK293 Cells

A Subset of GAF Domains Are Evolutionarily Conserved Sodium Sensors

Potent Inactivation-Dependent Inhibition of Adult and Neonatal NaV1.5 Channels by Lidocaine and Levobupivacaine