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Project

Molecular mechanisms of the interaction between neurotoxins and potassium and sodium channels.

This project focuses on the novel lipid exposed toxin/drug binding site in Kv channels that we recently characterized using the marine neurotoxin gambierol. This binding site is most likely the molecular equivalent of Nav channel 'site 5'. Site 5 (and site 2) toxins disrupt fast inactivation and cause a negative shift in the activation leading to persistent Na-current (i.e. potentiation). However, in Kv channels the toxin binding had an opposite effect and resulted in channel block. The overall goal is to expand our knowledge on this novel type of binding site(s) in Kv channels and unravel the molecular mechanism by which these toxins potentiate Nav channels but block Kv channels.
Date:1 Jan 2012 →  31 Dec 2015
Keywords:MOLECULAR BIOPHYSICS, MEDICAL BIOCHEMISTRY, NEUROTOXINS
Disciplines:Biophysics, Biomarker discovery and evaluation, Drug discovery and development, Medicinal products, Pharmaceutics, Pharmacognosy and phytochemistry, Pharmacology, Pharmacotherapy, Toxicology and toxinology, Other pharmaceutical sciences
Project type:Collaboration project