• Publications
  • Influence
In vivo cancer gene therapy by adenovirus-mediated transfer of a bifunctional yeast cytosine deaminase/uracil phosphoribosyltransferase fusion gene.
Direct transfer of prodrug activation systems into tumors was demonstrated to be an attractive method for the selective in vivo elimination of tumor cells. However, most current suicide gene therapyExpand
  • 195
  • 14
Inhibition of Calcineurin by FK506 Protects against Polyglutamine-Huntingtin Toxicity through an Increase of Huntingtin Phosphorylation at S421
  • R. Pardo, Emilie Colin, +4 authors F. Saudou
  • Biology, Medicine
  • The Journal of Neuroscience
  • 2006
Huntington’s disease (HD) is caused by an abnormal expanded polyglutamine (polyQ) repeat in the huntingtin protein. Insulin-like growth factor-1 acting through the prosurvival kinase Akt mediates theExpand
  • 120
  • 14
Interactions between NEEP21, GRIP1 and GluR2 regulate sorting and recycling of the glutamate receptor subunit GluR2
Trafficking of AMPA‐type glutamate receptors (AMPAR) between endosomes and the postsynaptic plasma membrane of neurons plays a central role in the control of synaptic strength associated withExpand
  • 112
  • 13
Akt is altered in an animal model of Huntington's disease and in patients
  • Emilie Colin, E. Régulier, +6 authors F. Saudou
  • Biology, Medicine
  • The European journal of neuroscience
  • 1 March 2005
The insulin‐like growth factor I (IGF‐1)/Akt pathway plays a crucial role in Huntington's disease by phosphorylating the causative protein, polyQ‐huntingtin, and abolishing its toxic properties [Expand
  • 157
  • 10
Hsp104 antagonizes alpha-synuclein aggregation and reduces dopaminergic degeneration in a rat model of Parkinson disease.
Parkinson disease (PD) is characterized by dopaminergic neurodegeneration and intracellular inclusions of alpha-synuclein amyloid fibers, which are stable and difficult to dissolve. WhetherExpand
  • 157
  • 7
Sensitive biochemical aggregate detection reveals aggregation onset before symptom development in cellular and murine models of Huntington’s disease
A CAG‐repeat gene expansion translated into a pathogenic polyglutamine stretch at the N‐terminus of huntingtin triggers Huntington’s Disease. Mutated huntingtin is predicted to adopt toxic propertiesExpand
  • 110
  • 7
MAP Kinase Phosphatase 1 (MKP-1/DUSP1) Is Neuroprotective in Huntington's Disease via Additive Effects of JNK and p38 Inhibition
We previously demonstrated that sodium butyrate is neuroprotective in Huntington's disease (HD) mice and that this therapeutic effect is associated with increased expression of mitogen-activatedExpand
  • 69
  • 6
Dysregulation of Gene Expression in Primary Neuron Models of Huntington's Disease Shows That Polyglutamine-Related Effects on the Striatal Transcriptome May Not Be Dependent on Brain Circuitry
Gene expression changes are a hallmark of the neuropathology of Huntington's disease (HD), but the exact molecular mechanisms of this effect remain uncertain. Here, we report that in vitro models ofExpand
  • 83
  • 4
Neuroprotection by Hsp104 and Hsp27 in lentiviral-based rat models of Huntington's disease.
Huntington's disease (HD) is an inherited neurodegenerative disorder caused by an expansion of glutamine repeats in the huntingtin (htt) protein. Abnormal protein folding and the accumulation ofExpand
  • 135
  • 3
Dose-dependent neuroprotective effect of ciliary neurotrophic factor delivered via tetracycline-regulated lentiviral vectors in the quinolinic acid rat model of Huntington's disease.
The ability to regulate gene expression constitutes a prerequisite for the development of gene therapy strategies aimed at the treatment of neurologic disorders. In the present work, we usedExpand
  • 108
  • 3