Magalie Ravier
  • E-mail :[email]
  • Phone : +33 4 34 35 92 03
  • Location : Montpellier, France
Last update 2017-09-01 10:16:16.797

Magalie Ravier PhD Endocrinology Diabetes

Course and current status

From 2015: Co-leader of the team physiopathology of pancreatic beta cells, Montpellier, France.

From 2009: Researcher, CR1 INSERM, Institut de Genomique Fonctionnelle, team physiopathology of pancreatic beta cells, Montpellier, France.
 

2006-2009: Postdoc in Jean-Claude Henquin's lab, University of Louvain, Unit of Endocrinology and Metabolism, Brussels, Belgium.
 

2002-2006: Postdoc in Guy A Rutter's lab (now in Imperial College London), University of Bristol, Department of Biochemistry in the laboratory , Bristol, UK.
 

1997-2002: PhD student in Jean-Claude Henquin's lab, University of Louvain, Unit of Endocrinology and Metabolism, Brussels, Belgium. « The oscillations of insulin secretion: triggering by cytosolic calcium and modulation by amplification systems in b cells»

Funding :

  • 2015: Université de Montpellier
  • 2012-2015: French National Research Agency (ANR)
  • 2011-2014: Fondation pour la Recherche Médicale (FRM)
  • 2010-2012: Société Francophone du Diabète
  • 2007-2008: Société Francophone du Diabète
  • 2006-2009: FNRS Fellowship


Awards :

  • 2011: Rising Star from European Association for the Study of Diabetes. 

https://www.easd.org/prizes.html

  • 2005: AREDIC (Association pour la Recherche sur le Diabète,

  

Scientific summary

Pancreatic ß-cells are the unique cells of the organism with the capacity to biosynthesize, store and secrete insulin in response to physiological needs. ß-cells play a central role in the etiology of Diabetes. Preservation or restoration of a functional ß-cell mass is essential. Our objectives, divided into basic research components and clinical investigation, are to examine the cellular and molecular mechanisms controlling function, survival and death of ß-cells, to investigate how these go awry in the pathogenesis of diabetes, and how stress and environnement influence ß-cell function and survival.

A better understanding of the signaling pathways linked to G-protein coupled receptors (GPCRs) and tyrosine kinase receptors (TKRs) in ß-cells is essential to identify new molecular targets to treat Diabetes with the aim to preserve or restore the functional ß-cell mass.

My specific aims are to identify the cellular and molecular mechanisms involved in the synergism between signaling pathways engaged by GPCRs (GLP-1 receptors, taken as drug targets for type 2 diabetes), TKRs (Insulin and IGF-1 receptors) and glucose in ß-cells.

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