A5023217404- Zebrafish Biomedical Research Applications
- Neuroinflammation and Neurodegeneration Mechanisms
- Prion Diseases and Protein Misfolding
- Retinal Diseases and Treatments
- Neurogenesis and neuroplasticity mechanisms
- Neurological Disease Mechanisms and Treatments
- Enzyme-mediated dye degradation
- Horticultural and Viticultural Research
- Nerve injury and regeneration
- Retinal Development and Disorders
- Plant Gene Expression Analysis
- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Trace Elements in Health
Université de Montpellier
2021
Inserm
2021
École Pratique des Hautes Études
2021
Mécanismes moléculaires dans les démences neurodégénératives
2020-2021
Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement
2020
Virologie et Immunologie Moléculaires
2017-2020
Institut Jean-Pierre Bourgin
2019
AgroParisTech
2019
Université Paris-Saclay
2017-2019
Centre National de la Recherche Scientifique
2019
Dedicated lignocellulosic feedstock from grass crops for biofuel production is extensively increasing. However, the access to fermentable cell wall sugars by carbohydrate degrading enzymes impeded lignins. These complex polymers are made reactive oxidized monolignols in wall. Little known about laccase-mediated oxidation of grasses, and inactivation monolignol polymerization mechanism might be a strategy increase yield sugars. LACCASE5 LACCASE8 inactivated Brachypodium double mutant....
Retinitis pigmentosa (RP) is one of the most common forms inherited retinal degeneration with 1/4,000 people being affected. The vision alteration primarily begins rod photoreceptor degeneration, then degenerative process continues cone death. Variants in 71 genes have been linked to RP. One these genes, PDE6a responsible for RP43. To date no treatment available and patients suffer from pronounced visual impairment early childhood. We used novel zebrafish pde6a Q70X mutant, generated by...
Prions result from a drastic conformational change of the host-encoded cellular prion protein (PrP), leading to formation β-sheet–rich, insoluble, and protease-resistant self-replicating assemblies (PrPSc). The molecular mechanisms involved in spontaneous sporadic inherited human diseases or equivalent animal are poorly understood, part because cell models spontaneously forming prions currently lacking. Here, extending studies on role H2 α-helix C terminus PrP, we found that deletion highly...
Mapping out regions of PrP influencing prion conversion remains a challenging issue complicated by the lack structure. The portion associated with infectivity contains α-helical domain correctly folded protein and turns into β-sheet-rich insoluble core in prions. Deletions performed so far inside this segment essentially prevented conversion. Recently we found that deletion last C-terminal residues helix H2 was fully compatible RK13-ovPrP cell culture model, using 3 different infecting...