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Professor Jules Hancox

I am interested in elucidating the function of small membrane proteins (ion channels and exchangers) responsible for generating electrical activity of cells in the heart. I have a long-standing interest is the basis of the activity of a key part of the heart's electrical conducting system called the atrioventricular (AV) node, which co-ordinates the normal sequence of beating of the heart's upper and lower chambers (the atria and ventricles). We study single AV node cells using electrophysiological and imaging techniques. Recent work in collaboration with Clive Orchard , Andrew James and Prof Godfrey Smith (Glasgow) has been focused on the effects of acidosis, endothelin-1 and calcium-cycling on AV node cellular electrophysiology. Collaborative work with colleagues in Manchester (Prof Mark Boyett, Prof Henggui Zhang) and Kings College London (Dr Oleg Aslanidi) is focused on producing biophysically accurate models of the AV node and atrium.

I also have a long-standing interest in the electrophysiology and pharmacology of the hERG potassium channel, which plays an important role in drug-induced arrhythmias and in the congenital 'Short QT syndrome'. Using a combination of molecular and electrophysiological methods, we have studied mechanisms of hERG blockade by a range of drugs and identified in vitro the antiarrhythmic disopyramide as an effective inhibitor of the hERG mutant K+ channel responsible for one form of Short QT syndrome. We are also investigating different K+ channel mutations involved in other forms of this syndrome and are focused both on identifying pharmacological agents that can inhibit Short QT mutant channels and on identifying arrhythmia substrates in the syndrome (in collaboration with Prof Henggui Zhang and colleagues, Manchester).

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Research keywords

  • cardio

Diseases related to this field of research

  • Hypertension

Processes and functions relevant to this work

  • Molecular microbiology

Equipment relevant to this work

  • Electrophysiological equipment

Research findings

  • Disruption of hERG function by extracellular acidosis reduces protection against a premature cardiac action potential Read more >


  • Dave Bates - Bristol
  • Mark Boyett - Manchester
  • Massimo Caputo - Bristol Heart Institute
  • Chris Dempsey - Biochemistry
  • Bristol Andrew James - Bristol
  • John Vann Jones
  • Cardiology
  • BRI
  • Bristol Clive Orchard - Bristol
  • Godfrey - Glasgow
  • Saadeh Suleiman - Bristol Heart Institute
  • Harry Witchel - Sussex
  • Henggui Zhang - Manchester