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Dr. Sebastien Jauliac


Brief Biography:

Sébastien Jauliac received a M2 degree from Pasteur Institute, University Pierre et Marie Curie, Paris, France in 1996 and a PhD from University Pierre et Marie Curie, Paris, France in 1999. He conducted his post-doctoral research in the laboratory of Prof. Alex Toker in the Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, US. His first faculty appointment was as INSERM Avenir Scientist at IUH, Paris, France in 2004, where he was promoted to Principal Investigator (CR1: Assistant Professor) in 2006.


Academic positions:

2004-2006: Avenir scientist INSERM

2006-now: Assistant professor INSERM


Research interests:

Our team works on the molecular mechanisms involved in breast cancer metastases formation. We study the role of NFAT transcription factors in the regulation of the migratory and invasive capacities of breast carcinoma, contributing to the formation of metastases. We currently work on both the identification of the mechanisms of NFAT transcription factors activation and the identification of their downstream genes required to increase or blunt the cellular motility. The goals of these studies is to be able to provide new therapeutic targets to prevent or cure breast cancer metastases. Our discovery of the expression and function of the NFAT transcription factors in breast cancer (Jauliac et al. 2002; Yeoli-Lerner et al., 2005; Fougère et al. 2010) has allowed for the first time to highlight the key role of these transcription factors in breast cancer biology and other cancers types (Bégué et al., 2012). Our team have identified key genes targeted by the NFAT transcription factors to modulate breast cancer carcinoma motility (Fougère et al., 2010; Germann et al., 2012; Gaudineau et al., 2012). Critically we have shown that depending on the NFAT isotype and the cellular context the consequences on genes regulation and cell motility can be completely divergent (Fougère et al., 2010; Gaudineau et al., 2012). Our studies have opened a new field of research in the study of cancers.

Selected Publications

- Lipocalin 2 (LCN2), the TNF-like receptor TWEAKR and its ligand TWEAK act downstream of NFAT1 to regulate breast cancer cell invasion. Benoît Gaudineau, Marjorie Fougère, Frédéric Guaddachi, Frédéric Lemoine, Pierre de la Grange and Sébastien Jauliac. Journal of Cell Science, 2012 jcs.105023; Advance Online Publication July 5, 2012, doi:10.1242/jcs.105023.

- Inducible expression and pathophysiological functions of T-plastin in cutaneous T-cell lymphoma. Elodie Bégué, Francette Jean-Louis, Martine Bagot, Sébastien Jauliac, Jean-Michel Cayuela, Liliane Laroche, Nathalie Parquet, Hervé Bachelez, Armand Bensussan, Gilles Courtois and Laurence Michel. Blood. 2012 May 24 , advance online publication; doi:10.1182/blood-2011-09-379156.

- Dual role of the ddx5/ddx17 RNA helicases in the control of the pro-migratory NFAT5 transcription factor. S Germann, L Gratadou, E Zonta, E Dardenne, B Gaudineau, M Fougère, S Samaan, M Dutertre, S Jauliac and D Auboeuf. Oncogene. 2012 January 23, advance online publication; doi:10.1038/onc.2011.618.

- NFAT3 transcription factor inhibits breast cancer cell motility by targeting the Lipocalin 2 gene. Fougère M, Gaudineau B, Barbier J, Guaddachi F, Feugeas JP, Auboeuf D, Jauliac S. Oncogene. 2010 Apr 15;29(15):2292-301.

- Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT. Yoeli-Lerner M, Yiu GK, Rabinovitz I, Erhardt P, Jauliac S, Toker A. Mol Cell. 2005 Nov 23;20(4):539-50.

- The role of NFAT transcription factors in integrin-mediated carcinoma invasion. Jauliac S, López-Rodriguez C, Shaw LM, Brown LF, Rao A, Toker A. Nat Cell Biol. 2002 Jul;4(7):540-4.


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