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Dr Anselm Zdebik
1-702 UCL Medical School, Royal Free Campus
Rowland Hill Street
  • Senior Lecturer
  • Neuro, Physiology & Pharmacology
  • Div of Biosciences
  • Faculty of Life Sciences
Medical education in Heidelberg, PhD in 1998, MD 2000
Clinical training at Freiburg University Hospital (Gastroenterology, Infectious diseases)
Physiology Freiburg University
2000-2008 Postdoc with Thomas J. Jentsch, Hamburg and Berlin
Research Summary
CLC proteins have been known as chloride channels for many years and have been implicated in a variety of diseases. KO mice for ClC-2, -3, and ClC-6 have revealed further interesting functions of this protein family. During my postdoctoral fellowship in Thomas Jentsch' laboratory (www.fmp-berlin.de/jentsch.html), I have worked on and generated several CLC-related knock-in mouse models.
After the discovery of chloride/proton antiport in a bacterial CLC homologue, Michael Puschs group (www.ge.cnr.it/ICB/conti_moran_pusch/programs-pusch/home-mik.htm) and ourselves found that ClC-4 and ClC-5 are exchangers rather than chloride channels. Chloride/proton antiport has recently also been shown for lysosomes expressing almost exclusively ClC-7 and its subunit, Ostm1. As revealed by single channel recordings of concatemeric CLC channels and bacterial crystal structures of CLC exchangers, these proteins function as dimers. CLC exchangers can be converted to pure anion conductances by neutralizing a "gating glutamate" conserved in (almost) all CLC proteins. This glutamate will open the chloride pathway when protonated in the wild-type transporter, thereby coupling anion to proton movement.
Teaching Summary
Physiology at Freiburg, Hamburg, Berlin (Max-Delbruck Centre). Since 2008 Lecturer, Neuroscience, Physiology and Pharmacology, UCL
Academic Background
  AFHEA ATQ02 - Recognised by the HEA as an Associate Fellow  
1998 MEd Master of Education – Medicine Ruprecht-Karls-Universit├Ąt Heidelberg
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