The Paris Cardiovascular Centre (PARCC), is an international research unit focusing on human pathophysiology, epidemiology, genomics and personalised medicine at the Institut National de la Santé et de la Recherche Médicale (INSERM) and the University of Paris - a leading French university with a strong commitment to life science research.

The Tharaux lab has a postdoctoral position available to study the pathophysiology of kidney diseases.

The successful applicant will work within an established group actively involved in preclinical and translational research on glomerular diseases.

http://parcc.inserm.fr/research-teams/team/tharaux-camerer/

The team will compare signaling pathways in mouse models of human diseases and human tissues, address data integration, analysis and interpretation challenges stemming from time-resolved data generated in clinical and research settings. Specific application areas include kidney diseases. The Fellow will work on projects such as multimodal joint learning from preclinical biological and imaging data.

Candidates with experience in biochemistry, cell and molecular biology, signal transduction, cytoskeletal dynamics, and/or animal models will be given preference. Attention to detail and good communication/interpersonal skills is critical as well as oral and written communication skills in English and ability to work as a part of an interdisciplinary team.

Knowledge of tissue imaging or RNA sequencing or proteomics analyses is a plus.

Salary will be commensurate to previous experience and in line with EU standards. The position is to be filled by December 2019.

Please send a cover letter (explaining your specific interests in our research! as well as the names of at least two academic references) and a CV to Pierre-Louis Tharaux at pierre-louis.tharaux@inserm.fr

Selected publications:

-The tetraspanin CD9 controls invasive migration and proliferation of parietal epithelial cells and glomerular disease progression. Lazareth H, Hénique C, Lenoir, Puelles VG et al. Nat Commun. 2019, in press

-Genetic and Pharmacological Inhibition of MicroRNA-92a Maintains Podocyte Cell Cycle Quiescence and Limits Crescentic Glomerulonephritis.  Hénique C, et al. Nat Commun. 2017 28;8(1):1829

-Nrf2 drives podocyte-specific PPAR expression that is essential to promote resistance to crescentic glomerulonephritis.  Hénique C & Bollee G et al. J Am Soc Nephrol. 2016;27(1):172-88.

-Endothelial cell- and podocyte autophagy synergistically protect from diabetes-induced glomerulosclerosis. Lenoir O, et al. Autophagy. 2015;11(7):1130-45

-The Epidermal Growth Factor Receptor Promotes Glomerular Injury and Renal Failure in Rapidly Progressive Crescentic Glomerulonephritis. Bollée G & Flamant M et al.

Nat Med. 2011;17(10):1242-50.