Area of research
Physiology · Cellular and Molecular Neuroscience
Research interest
Research interests include Pain Mechanisms and Treatments, Axon Guidance and Neuronal Signaling, Ion channel regulation and function, and Neurofibromatosis and Schwannoma Cases.
The natural product argentatin C attenuates postoperative pain via inhibition of voltage‐gated sodium and T‐type voltage‐gated calcium channels
Targeting T-type/CaV3.2 channels for chronic pain
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
SARS-CoV-2 spike protein co-opts VEGF-A/neuropilin-1 receptor signaling to induce analgesia
Studies on CRMP2 SUMOylation–deficient transgenic mice identify sex-specific Nav1.7 regulation in the pathogenesis of chronic neuropathic pain
The Natural Flavonoid Naringenin Elicits Analgesia through Inhibition of NaV1.8 Voltage-Gated Sodium Channels
Reversal of Peripheral Neuropathic Pain by the Small-Molecule Natural Product Physalin F via Block of CaV2.3 (R-Type) and CaV2.2 (N-Type) Voltage-Gated Calcium Channels
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
A porcine model of neurofibromatosis type 1 that mimics the human disease
A Modular Assembly of Spinal Cord–Like Tissue Allows Targeted Tissue Repair in the Transected Spinal Cord
CRMP2–Neurofibromin Interface Drives NF1-related Pain
High Fidelity Cryopreservation and Recovery of Primary Rodent Cortical Neurons
(−)-Hardwickiic Acid and Hautriwaic Acid Induce Antinociception via Blockade of Tetrodotoxin-Sensitive Voltage-Dependent Sodium Channels
Cholestane-3β, 5α, 6β-triol suppresses neuronal hyperexcitability via binding to voltage-gated 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
Dissecting the role of the CRMP2–neurofibromin complex on pain behaviors
Homology‐guided mutational analysis reveals the functional requirements for antinociceptive specificity of collapsin response mediator protein 2‐derived peptides
CRMP2 is necessary for Neurofibromatosis type 1 related pain