Emilie LEMESRE

En résumé

Entreprises

• Inserm - Chercheur

  PARIS 13 2017 - 2018 I use a synchronization assay to study the role of dymeclin on the transport of post-Golgi vesicles in neurons and oligodendrocytes. Dymeclin, whose function is still unknown, is the protein involved in an autosomal recessive skeletal dysplasia associated with microcephaly and intellectual disability called the Dyggve-Melchior-Clausen syndrom (DMC). Its association with Golgi membrane argue for a role of Dymeclin in Golgi homeostasis and/or Golgi-associated vesicular trafficking.

• Institut Curie/UMR 144 - Post-doctoral researcher

  2012 - 2016 I use the synchronization assay developed in the lab to study the transport of
  rhodopsin to the primary cilium of stable cell line by time-lapse microscopy.
  I develop a new approach combined to the synchronization system to generate
  time-lapse maps of the protein landscape met by secretory proteins during their
  transport without relying of subcellular fractionation.

• JUle Stein Eye Institute/UCLA - Post-doctoral researcher

  2008 - 2012 I develop a FRAP based assay on primary cilium of various cell line to study the
  transport of rhodopsin

Formations

• Institut Curie / UMR

  Paris 2003 - 2008 doctorat
  
  intracellulaire et mort neuronale
  Caractérisation du rôle neuro-protecteur de la voie de signalisation induite
  par IGF-1 dans la maladie de Huntington:
  * Altération de l'expression et de l'activation d'Akt dans un modèle de la
  maladie et chez les patients
  * Rôle de la phosphorylation de la huntingtine à la sérine 421 dans le
  transport intracellulaire.

• Université Paris XI Paris Sud

  Orsay 2003 - 2007 Neurobiology PhD
  
  I demonstrate that Akt is altered in an animal model of Huntington’s disease and in
  peripheral tissues of patients before neurodegeneration.
  I demonstrate that the phosphorylation of huntingtin at Serine 421 by IGF-1/Akt
  signaling pathway is neuroprotective in vivo.
  I participate to the study showing that Calcineurin is the phosphatase that
  dephosphorylates huntingtin at Serine 421.
  I show that th

• Université Paris VII

  Paris 2002 - 2003 DEA

• Institut Curie / UMR

  Paris 2002 - 2003

• Université Paris XI

  Paris 2001 - 2002 Maîtrise de Biologie Cellulaire et Physiologie
  
  Module : Génétique Humaine

• Université Poitiers

  Poitiers 2000 - 2001 Maîtrise de Biologie Cellulaire et Physiologie

• Université Poitiers

  Poitiers 1999 - 2000 Licence de Biologie Cellulaire et Moléculaire

• Université Poitiers

  Poitiers 1998 - 1999 2 ème année du DEUG

• Université De Poitiers Médecine

  Poitiers 1997 - 1998 PCEM1

• Université Poitiers

  Poitiers 1996 - 1997 PCEM1

• Lycée Guez De Balzac

  Angouleme 1995 - 1996 Baccalauréat S

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