Thomas J. Jentsch
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Thomas J. Jentsch | |
|---|---|
| Born | Germany |
| Education | Dr. rer. nat., Dr. med. |
| Alma mater | Freie Universität Berlin |
| Known for | Discovery and characterization of CLC chloride channels/Cl⁻/H⁺ exchangers; volume-regulated anion channels (VRAC); acid-activated anion channel (ASOR/TMEM206) |
| Awards | Gottfried Wilhelm Leibniz Prize, Louis-Jeantet Prize. |
| Scientific career | |
| Fields | Ion channel biology, chloride channels (CLC family) |
| Institutions | Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Max-Delbrück-Center for Molecular Medicine |
Thomas J. Jentsch (born April 24, 1953) is a German molecular physiologist and expert in ion‑transport biology whose work has helped shape the understanding of chloride channel families and their role in human physiology and disease.[1] 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/Cl⁻/H⁺‑exchanger) gene family, the discovery of their roles in human disorders (such as myotonia, osteopetrosis, kidney disease), and the more recent identification of volume‑regulated anion channels (VRAC) and acid‑activated anion channels (ASOR).[2][3]
Thomas J. Jentsch studied both medicine and physics at the Freie Universität Berlin.[3] He obtained doctoral degrees in both the Dr. rer. nat. (physics) and the Dr. med. (medicine) at the same institution.[2] Following his doctoral work, Jentsch carried out post‑doctoral research in transport physiology in Berlin and at the Whitehead Institute/ MIT in the United States, working with Harvey Lodish.[3]
Research and career
In 1988 Jentsch was a founding member of the Center for Molecular Neurobiology Hamburg (ZMNH).[3] In 2006 he moved his laboratory to Berlin, joining the FMP and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC).[3] His laboratory's research spans from molecular and structural biology of ion channels to their integration in cell biology, physiology and disease.[2] Jentsch's group made contributions to the identification and functional analysis of the CLC family of chloride channels and Cl⁻/H⁺ exchangers in mammals.[4] They also more recently found that the volume‑regulated anion channel (VRAC) is composed of LRRC8 heteromers and that an acid‑activated anion channel (ASOR/TMEM206) is another key Cl⁻ channel with physiological relevance.[3]
Major discoveries and contributions
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 plasma‑membrane chloride channels regulating membrane excitability to intracellular Cl⁻/H⁺ exchangers modulating endolysosomal acidification.[4] His 2015 review “Discovery of CLC transport proteins: cloning, structure, function and pathophysiology” outlines the path from ClC‑0 to a broad understanding of ion transport and disease.[2] His work demonstrated that mutations in CLC genes underlie a range of human genetic diseases - for example, myotonia congenita (CLCN1), Bartter syndrome (ClC‑K/barttin), osteopetrosis (ClC‑7/Ostm1) - thereby linking basic channel biology to translational and clinical relevance.[2] Through his structural‑functional 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.[5]
