Department Physiology and Pathology of Ion Transport (Thomas J. Jentsch)
Our group belongs both to the MDC and the FMP and is located in the new Timoféeff-Ressovsky-Haus on the campus Berlin-Buch in Berlin.
Prof. Thomas J. Jentsch
Phone: +49-30-9406-2961 Fax: +49-30-9406-2960
jentsch(at)fmp-berlin.de
Research Coordinator Dr. Dietmar Zimmer
Phone: +49-30-9406-2974 Fax: +49-30-9406-2960
dietmar.zimmer(at)mdc-berlin.de
Prof. Thomas J. Jentsch
1982 Ph.D. (physics) Freie Universität Berlin and Fritz-Haber-Institut der Max-Planck-Gesellschaft.
1984 M.D. Freie Universität Berlin
Doctoral and postdoctoral work at the Institut für Klinische Physiologie, Freie Universität Berlin
Postdoctoral work with Harvey Lodish at the Whitehead Institute for Biomedical Research (MIT) 1986-1988
Research Group Leader at the ZMNH, Hamburg University 1988 - 1993
Full professor and Director of the Institute for Molecular Neuropathology at the ZMNH 1993-2006
Director of the ZMNH, 1995-1998, 2001-2003
2006- Full professor at the Charité Berlin, Head of research group Physiology and Pathology of Ion Transport at the FMP (Leibniz-Institut für Molekulare Pharmakologie) and MDC (Max-Delbrück-Centrum für Molekulare Medizin)
2008- Principal Investigator of Neurocure
Awards / Honours
Research overview
Ion transport processes play crucial roles in neuronal excitability, signal transduction, transport of salt, water, and other substances across epithelia, and the homeostasis of extracellular, cytosolic, and vesicular compartments.
Our investigations stretch from structure-function studies and biophysis to cell biological aspects like endocytosis and to the physiological and systemic role of particular transport proteins. We have identified several human genetic diseases that are due to mutations in ion channels and have generated various knock-out mouse models. Their phenotypes yield important insights into the normal role of particular ion transporters and indicate candidate genes for human diseases. In accord with the broad importance of ion transport, these disorders include epilepsy and neurodegeneration, deafness, kidney stones, urinary protein loss, hypertension, and thick bones (osteopetrosis), among others. Our work bridges the gap between molecular studies and systems biology.
We investigate the functions of CLC chloride channels and transporter, KCNQ potassium channels, KCC K-Cl-cotransporters, and have recently begun to study also Ca-activated chloride channels.
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BACK TO CLASSICS. In the classical picture of vesicular acidification, electrical currents of the H+-ATPase are neutralized by a Cl- channel (left). However, we have shown that endosomal CLC proteins, instead of being Cl- channels, are rather Cl-/H+ exchangers (centre), raising the question what this exchange is good for. In our most recent work, we generated knock-in mice in which we converted selected CLC exchangers into channels using single point mutations (right panel). These mice should display normal acidification of endosomes (for ClC-5) or lysosomes (for ClC-7). Surprisingly, both mouse models (Clcn5unc and Clcn7unc, unc for uncoupled from protons) display phenotypes (impaired endocytosis or neurodegeneration) that largely overlap with those of the respective KOs. We suggest that there is an important, previously unrecognized role of luminal chloride concentration. These exciting results, which have profound implications for cell biology of endolysosomal trafficking and function, have just been published in Science. See Weinert et al. and Novarino et al.
