Bethan Cole on Muck Rack

Bethan Cole

Shrewsbury
As seen in: Financial Times, MDPI, VICE, ELLE, British GQ, British Vogue, Cell Press, Glamour (UK), Vogue Japan, Electronic Sound and
Writer and editor; cat, hedgehog, puffin and moomin lover. Contributing to Vogue Japan, Glamour, Red. Memoir (Everywhere is) Closed on Sundays - is on Amazon.
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Articles

Identification of new KCNT1-epilepsy drugs by in silico, cell and Drosophila modelling.

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By Michael G Ricos, Bethan Cole, Rashid Hussain, Grigori Rychkov
| biorxiv.org
Abstract Objective: Hyperactive KCNT1 potassium channels, caused by gain-of-function mutations, are associated with a range of epilepsy disorders. Patients typically experience drug-resistant seizures and in cases with infantile onset, developmental regression can follow. KCNT1-related disorders include epilepsy of infancy with migrating focal seizures and sleep related hypermotor epilepsy.
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A molecular switch in RCK2 triggers sodium-dependent activation of KNa1.1 (KCNT1) potassium channels

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By Bethan Cole, Antreas C. Kalli, Nadia Pilati, Autifony Srl
| Cell Press
Results 17 Zhang Z. Rosenhouse-Dantsker A. Logothetis D.E. et al. The RCK2 domain uses a coordination site present in Kir channels to confer sodium sensitivity to Slo2.2 channels. J. Neurosci.
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A molecular switch in RCK2 triggers sodium-dependent activation of KNa1.1 (KCNT1) potassium channels.

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By Bethan Cole, Antreas C. Kalli, Nadia Pilati, Stephen P. Muench
| biorxiv.org
Abstract The Na+-activated K+ channel KNa1.1, encoded by the KCNT1 gene, is an important regulator of neuronal excitability. How intracellular Na+ ions bind and increase channel activity is not well understood.
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See all 16 licensed articles (23 Total)

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