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School of Biological and Behavioural Sciences

Hannah Lee


PhD Student



Project Title: Investigation of Novel Molecular Mechanisms for Regulation of Neuronal Calcium Channels


Dysfunction and dysregulation of CaV channels has been implicated in a variety of physiological conditions, including chronic neuropathic pain, and the α2δ-1 subunit has been repeatedly implicated in chronic neuropathic pain pathways. α2δ-1 expression is essential for CaV channel function, increasing channel currents and trafficking of channels to cell membranes. Post-translational cleavage of α2δ into α2 and δ (which remain linked by a disulphide bonds) is essential for the facilitatory effect of α2δ on CaV channel function, and that prevention of α2δ cleavage reversibly inhibits CaV2.2 channel function. This suggests that proteolytic maturation of α2δ may play a key role in post-translational regulation of CaV channels. This indicates that if this cleavage process (which appears to act as a checkpoint) can be regulated, CaV channel function (and thus potentially neuropathic pain onset and maintenance) could also be regulated.

The project aims to investigate how the disulphide bridge between α2 and δ affects the biological functions of α2δ, and hence the post-translational regulation mechanisms of CaV channel function, in both heterologous expression systems and native primary hippocampal or DRG neurons. 



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