Biography Lucie Pellissier

2005: M. Sc. in Neurobiology, University of Montpellier 2, Montpellier, France.

2009: PhD in Neurobiology, University of Montpellier 1, Montpellier, France.

2009: Postdoctoral Fellow, Department of Neuromedical Genetics, The Netherlands Institute for Neurosciences (NIN), Royal Netherlands Academy of Arts and Sciences (KNAW), Amsterdam, The Netherlands.

Publications Lucie Pellissier

Barthet G, Carrat G, Cassier E, Barker B, Gaven F, Pillot M, Framery B, Pellissier LP, Augier J, Kang DS, Claeysen S, Reiter E, Banères JL, Benovic JL, Marin P, Bockaert J, Dumuis A. beta-arrestin1 phosphorylation by GRK5 regulates G protein-independent 5-HT(4) receptor signalling. EMBO J. 2009 Aug 6.
Pellissier LP, Sallander J, Campillo M, Gaven F, Queffeulou E, Pillot M, Dumuis A, Claeysen S, Bockaert J, Pardo L.Conformational toggle switches implicated in basal constitutive and agonist-induced activated states of 5-hydroxytryptamine-4 receptors.Mol Pharmacol. 2009 Apr;75(4):982-90.
Chang WC, Ng JK, Nguyen T, Pellissier L, Claeysen S, Hsiao EC, Conklin BR. Modifying Ligand-induced and Constitutive Signaling of the Human 5-HT4 Receptor. PLoS ONE. 2007 Dec 19;2(12):e1317.
Barthet G, Framery B, Gaven F, Pellissier L, Reiter E, Claeysen S, Bockaert J and Dumuis A. 5-HT4 receptor Activation of the ERK Pathway Depends on Src Activation but Not on G Protein or b-Arrestin signalling. Mol Biol Cell. 2007 Jun;18(6):1979-91.


Personal Interests

My main interest is to work on developing gene therapy using promising virus vectors.
During my phD and master studies, I studied the behavior of a new pharmacological tool, a GPCR insensible to its endogenous ligand. By viral vector, we introduced this gene to protect dopaminergic neurons in an in vitro neurodegenerative model of Parkinson's disease.
My postdoctoral interest is to extend my competence in in vivo therapeutic studies.
The aim of our current project is to develop a crumbs (Crb1) human gene therapy. Mutations in this protein lead to retinitis pigmentosa (RP) and Leber congenital Amaurosis (LCA). Using AAV particles, restoring Crb1expression in Muller glial cells will protect photoreceptors degeneration in Crb1 deficient mice and humans.