Thomasâ¯J.â¯Jentsch (born April 24, 1953) is a German molecular physiologist and expert in ionâÂÂtransport biology whose work has helped shape the understanding of chloride channel families and their role in human physiology and disease. He leads the Section for Physiology and Pathology of Ion Transport at the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) in Berlin and is affiliated with the Max Delbrück Center for Molecular Medicine. His research includes the cloning, structural and functional characterisation of the CLC (chloride channel/Clâ»/HâºâÂÂexchanger) gene family, the discovery of their roles in human disorders (such as myotonia, osteopetrosis, kidney disease), and the more recent identification of volumeâÂÂregulated anion channels (VRAC) and acidâÂÂactivated anion channels (ASOR).
Thomasâ¯J.â¯Jentsch studied both medicine and physics at the Freie Universität Berlin. He obtained doctoral degrees in both the Dr.â¯rer.â¯nat. (physics) and the Dr.â¯med. (medicine) at the same institution. Following his doctoral work, Jentsch carried out postâÂÂdoctoral research in transport physiology in Berlin and at the Whitehead Institute/ MIT in the United States, working with Harvey Lodish.
In 1988 Jentsch was a founding member of the Center for Molecular Neurobiology Hamburg (ZMNH). In 2006 he moved his laboratory to Berlin, joining the FMP and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC). His laboratory's research spans from molecular and structural biology of ion channels to their integration in cell biology, physiology and disease. Jentsch's group made contributions to the identification and functional analysis of the CLC family of chloride channels and Clâ»/H⺠exchangers in mammals. They also more recently found that the volumeâÂÂregulated anion channel (VRAC) is composed of LRRC8 heteromers and that an acidâÂÂactivated anion channel (ASOR/TMEM206) is another key Clâ» channel with physiological relevance.
One of Jentsch's main achievements is the cloning and characterisation of the CLC gene family, which comprises nine members in humans and reveals a dramatic diversity of function, from plasmaâÂÂmembrane chloride channels regulating membrane excitability to intracellular Clâ»/H⺠exchangers modulating endolysosomal acidification. His 2015 review âÂÂDiscovery of CLC transport proteins: cloning, structure, function and pathophysiologyâ outlines the path from ClCâÂÂ0 to a broad understanding of ion transport and disease. His work demonstrated that mutations in CLC genes underlie a range of human genetic diseases - for example, myotonia congenita (CLCN1), Bartter syndrome (ClCâÂÂK/barttin), osteopetrosis (ClCâÂÂ7/Ostm1) - thereby linking basic channel biology to translational and clinical relevance. Through his structuralâÂÂfunctional studies, Jentsch helped reveal how channel architecture controls transport properties, and how intracellular chloride channels contribute to vesicular and lysosomal function, neuronal health, bone resorption, and kidney physiology.
Thomas J. Jentsch has received numerous awards over his career, reflecting contributions to ion-channel biology. In 1995, he was awarded the Gottfried Wilhelm Leibniz Prize by the German Research Foundation (DFG) for his work on chloride channels. He has been awarded European Research Council (ERC) Advanced Grants, first in 2011 and again in 2017. In recognition of his scientific achievements, he was granted an Honorary Doctorate (Dr. h.c.) by the University Medical Center Hamburg-Eppendorf in 2017. He has also received the Hodgkin-Huxley-Katz Prize Lecture (2006), Adolf-Fick Prize (2004), Homer W. Smith Award for Nephrology (2004), and the Ernst Jung Prize for medicine (2001). In 2018, he was awarded the âÂÂGesellschaft braucht Wissenschaftâ (âÂÂSociety needs ScienceâÂÂ) Prize by the Stifterverband, and in 2024 he became an Honorary Member of the German Physiological Society. In 2000, Jentsch was awarded the Louis-Jeantet Prize for Medicine by the Fondation Louis-Jeantet. He is also a member of the Berlin-Brandenburg Academy of Sciences and Humanities.