Area of research
Physiology · Cellular and Molecular Neuroscience
Research interest
Research interests include Medicine, Neuropathic pain, Neuroscience, Nociception, Pharmacology, and Cell biology.
Robust cone-mediated signaling persists late into rod photoreceptor degeneration
Selective targeting of NaV1.7 via inhibition of the CRMP2-Ubc9 interaction reduces pain in rodents
Conotoxin contulakin-G engages a neurotensin receptor 2/R-type calcium channel (Cav2.3) pathway to mediate spinal antinociception
Studies on CRMP2 SUMOylation–deficient transgenic mice identify sex-specific Nav1.7 regulation in the pathogenesis of chronic neuropathic pain
Targeting the CaVα–CaVβ interaction yields an antagonist of the N-type CaV2.2 channel with broad antinociceptive efficacy
Mining the Nav1.7 interactome: Opportunities for chronic pain therapeutics
Development and Characterization of An Injury-free Model of Functional Pain in Rats by Exposure to Red Light
Tetramethylpyrazine Reduces Epileptogenesis Progression in Electrical Kindling Models by Modulating Hippocampal Excitatory Neurotransmission
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
CRMP2 and voltage-gated ion channels: potential roles in neuropathic pain
CRISPR/Cas9 editing of Nf1 gene identifies CRMP2 as a therapeutic target in neurofibromatosis type 1-related pain that is reversed by (S)-Lacosamide
Dissecting the role of the CRMP2–neurofibromin complex on pain behaviors
Long-lasting antinociceptive effects of green light in acute and chronic pain in rats
(S)-lacosamide inhibition of CRMP2 phosphorylation reduces postoperative and neuropathic pain behaviors through distinct classes of sensory neurons identified by constellation pharmacology
(S)-Lacosamide Binding to Collapsin Response Mediator Protein 2 (CRMP2) Regulates CaV2.2 Activity by Subverting Its Phosphorylation by Cdk5