Area of research
Physiology · Cellular and Molecular Neuroscience
Research interest
Research interests include Medicine, Sodium channel, Pharmacology, Neuroscience, Biology, and Neuropathic pain.
Human Hsp70 Substrate-Binding Domains Recognize Distinct Client Proteins
Identification and targeting of a unique Na <sub>V</sub> 1.7 domain driving chronic pain
A peptidomimetic modulator of the Ca <sub>V</sub> 2.2 N-type calcium channel for chronic pain
Animal Models of Neurodegenerative Disease: Recent Advances in Fly Highlight Innovative Approaches to Drug Discovery
Heat shock protein Grp78/BiP/HspA5 binds directly to TDP-43 and mitigates toxicity associated with disease pathology
Selective targeting of NaV1.7 via inhibition of the CRMP2-Ubc9 interaction reduces pain in rodents
<i>In Silico</i> Targeting of the Long Noncoding RNA MALAT1
Antihypertensive drug treatment and susceptibility to SARS-CoV-2 infection in human PSC-derived cardiomyocytes and primary endothelial cells
Direct targeting of TDP-43, from small molecules to biologics: the therapeutic landscape
Discovery and Characterization of 2,5-Substituted Benzoic Acid Dual Inhibitors of the Anti-apoptotic Mcl-1 and Bfl-1 Proteins
An Allosteric Modulator of RNA Binding Targeting the N-Terminal Domain of TDP-43 Yields Neuroprotective Properties
Structural Insights Into TDP-43 and Effects of Post-translational Modifications
Small Molecule Targeting TDP-43’s RNA Recognition Motifs Reduces Locomotor Defects in a <i>Drosophila</i> Model of Amyotrophic Lateral Sclerosis (ALS)
The Natural Flavonoid Naringenin Elicits Analgesia through Inhibition of NaV1.8 Voltage-Gated Sodium Channels
Targeting the CaVα–CaVβ interaction yields an antagonist of the N-type CaV2.2 channel with broad antinociceptive efficacy
Inhibition of the Ubc9 E2 SUMO-conjugating enzyme–CRMP2 interaction decreases NaV1.7 currents and reverses experimental neuropathic pain
Betulinic acid, derived from the desert lavender Hyptis emoryi, attenuates paclitaxel-, HIV-, and nerve injury–associated peripheral sensory neuropathy via block of N- and T-type calcium channels
(−)-Hardwickiic Acid and Hautriwaic Acid Induce Antinociception via Blockade of Tetrodotoxin-Sensitive Voltage-Dependent Sodium Channels
CRISPR/Cas9 editing of Nf1 gene identifies CRMP2 as a therapeutic target in neurofibromatosis type 1-related pain that is reversed by (S)-Lacosamide
Blocking CRMP2 SUMOylation reverses neuropathic pain
Homology‐guided mutational analysis reveals the functional requirements for antinociceptive specificity of collapsin response mediator protein 2‐derived peptides
A single structurally conserved SUMOylation site in CRMP2 controls NaV1.7 function
Hierarchical CRMP2 posttranslational modifications control NaV1.7 function
(S)-lacosamide inhibition of CRMP2 phosphorylation reduces postoperative and neuropathic pain behaviors through distinct classes of sensory neurons identified by constellation pharmacology
A membrane-delimited N-myristoylated CRMP2 peptide aptamer inhibits CaV2.2 trafficking and reverses inflammatory and postoperative pain behaviors
(S)-Lacosamide Binding to Collapsin Response Mediator Protein 2 (CRMP2) Regulates CaV2.2 Activity by Subverting Its Phosphorylation by Cdk5
Differential neuroprotective potential of CRMP2 peptide aptamers conjugated to cationic, hydrophobic, and amphipathic cell penetrating peptides
The functionalized amino acid (S)-Lacosamide subverts CRMP2-mediated tubulin polymerization to prevent constitutive and activity-dependent increase in neurite outgrowth