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The Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) belongs to the „Forschungsverbund Berlin e. V. (FVB)“. The FVB is an institution of eight natural sciences research institutes in Berlin funded by the Federal Republic of Germany and the association of its federal states. The research institutes are members of the Leibniz association.

In the group Physiologie und Pathologie des Ionentransportes (led by  Prof. Thomas Jentsch  ; FMP / MDC Berlin) there is an opening for


Postdocs in Electrophysiology and/or Cell Biology   (f/m/d)

(Ref. 30/2019 sowie 05/2020)


In ERC- and DFG-funded projects, we investigate the structure-function, cell biology and physiology of anion channels in cell culture and in newly generated genetic mouse models. Projects are focused on the newly identified ASOR/TMEM206 and VRAC/LRRC8 channels, and on selected members of the CLC family of chloride channels and transporters. Intriguingly, VRAC channels not only transport chloride, but also organic molecules including neurotransmitters and drugs.

We are an international, highly interdisciplinary group with a strong interest in elucidating the role of anion channels in the physiology and pathology of various organs, which include e.g. the brain, endocrine cells, and the kidneyOur lab is well equipped with several patch-clamp setups, ion imaging, confocal microscopy and all common equipment for molecular cell biology and morphology. We have direct access to the outstanding core facilities of the FMP and the MDC. 

We are looking for highly motivated young scientists with a solid background in physiology and cell biology and a keen interest in science. For the first position, we expect previous experience in electrophysiology, preferably in patch-clamp analysis of tissue (e.g. brain) slices, or alternatively in structure-function analysis of channels. Experience in ion concentration imaging and/or programming would be an asset. The successful candidate will have the opportunity to extend her/his expertise to other areas in molecular and cell physiology.

For the second position, the ideal candidate should have solid practical experience and theoretical background in cell biology, and preferably also in physiology and histology. Previous experience in the study of intracellular organelles and trafficking would be an asset as an important focus of our work concerns ion transport in endolysosomes.

Both positions are available immediately. The positions are limited for 2 years with an option for extension.  

Salaries will be based on TVöD Bund. In 2013 the institute has been awarded the certificate of the audit Beruf und Familie as family-friendly employer. We offer equal opportunities regardless of gender and welcome applications of disabled candidates. They will be preferred in case of equal qualification. We welcome applications from all backrounds.

Visit our webpage  to know more about our lab

On the FMP homepage please go to “Stellenangebote/Jobs” and click first on this advertisement and then on the button “Online bewerben”. Please combine your application documents including motivation letter, CV, names and contacts of references and copies of degree certificates as soon as possible but not later than February 29th  2020.


We are looking forward to your application!



Selected recent publications:

Voss F.K., Ullrich F., Münch J., Lazarow K., Lutter D., Mah N., Andrade-Navarro M.A., von Kries J.P., Stauber T., Jentsch T.J. (2014). Identification of LRRC8 heteromers as an essential component of the volume-regulated anion channel VRAC. Science 344, 634638.

Stuhlmann T., Planells-Cases R., Jentsch T.J. (2018). LRRC8/VRAC anion channels enhance β-cell glucose sensing and insulin secretion. Nature Communications 9:1974

Ullrich F., Blin S., Lazarow K., Daubitz T., von Kries J.P., Jentsch T.J. (2019). Identification of TMEM206 proteins as pore of PAORAC/ASOR acid-sensitive chloride channels. eLife 8.

Göppner C., Orozco I.J., Hoegg-Beiler M.B., Soria A.H., Hübner C.A., Fernandes-Rosa F.L., Boulkroun S., Zennaro M.C., Jentsch T.J. (2019). Pathogenesis of hypertension in a mouse model for CLCN2-related hyperaldosteronism. Nature Communications 10: 4678.