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Brid P Callaghan

Researcher at RMIT University

Publications -  15
Citations -  949

Brid P Callaghan is an academic researcher from RMIT University. The author has contributed to research in topics: Conotoxin & Nicotinic agonist. The author has an hindex of 11, co-authored 15 publications receiving 859 citations. Previous affiliations of Brid P Callaghan include University of Queensland & University of Wollongong.

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The engineering of an orally active conotoxin for the treatment of neuropathic pain

TL;DR: A new orally active conotoxin was developed to solve the problems of short biological half-lives and poor activity when taken orally in cone snail venoms.
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Analgesic alpha-conotoxins Vc1.1 and Rg1A inhibit N-type calcium channels in rat sensory neurons via GABAB receptor activation.

TL;DR: A novel mechanism by which α-conotoxins Vc1.1 and Rg1A modulate native N-type (CaV2.2) Ca2+ channel currents, namely acting as agonists via G-protein-coupled GABAB receptors is proposed, potentially mediating their analgesic actions.
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A novel mechanism of inhibition of high-voltage activated calcium channels by α-conotoxins contributes to relief of nerve injury-induced neuropathic pain

TL;DR: The findings suggest that inhibition of α9α10 nAChR is neither necessary nor sufficient for relief of allodynia and establish that α‐conotoxins selective for GABAB receptor‐dependent inhibition of N‐type Ca2+ channels relieve allodynian, and could therefore be developed to manage chronic pain.
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Total Synthesis of the Analgesic Conotoxin MrVIB through Selenocysteine‐Assisted Folding

TL;DR: Selenocysteine residues were used to drive the folding of conotoxin MrVIB, a previously "unfoldable" miniprotein with therapeutic potential and should generally facilitate the fold of peptides and proteins with multiple disulfide bonds.
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Analgesic conotoxins: block and G protein‐coupled receptor modulation of N‐type (CaV2.2) calcium channels

TL;DR: A series of newly discovered ω‐conotoxins from Conus catus, including CVID–F, are potent and selective antagonists of N‐type VGCCs and will lead to new ways to regulate VGCC block and modulation in normal and diseased states of the nervous system.