A5011145148- Alzheimer's disease research and treatments
- Endoplasmic Reticulum Stress and Disease
- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- Neuroscience and Neuropharmacology Research
- Hepatitis B Virus Studies
- Ion channel regulation and function
- Cholinesterase and Neurodegenerative Diseases
- Cell death mechanisms and regulation
- Extracellular vesicles in disease
- RNA regulation and disease
- Hepatitis C virus research
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Cellular transport and secretion
- Nicotinic Acetylcholine Receptors Study
- RNA Interference and Gene Delivery
- Peptidase Inhibition and Analysis
- Protein Kinase Regulation and GTPase Signaling
- RNA modifications and cancer
- RNA Research and Splicing
- Cannabis and Cannabinoid Research
- Liver Disease Diagnosis and Treatment
- Blood Pressure and Hypertension Studies
- Ion Channels and Receptors
- Flavonoids in Medical Research
Université Côte d'Azur
2012-2025
Inserm
2012-2025
Centre National de la Recherche Scientifique
2015-2025
Institut de Pharmacologie Moléculaire et Cellulaire
2014-2024
Institut de Biologie Valrose
2023
University of Ferrara
2002-2017
Centre Hospitalier de Bigorre
2016
Fondation pour la Recherche Médicale
2012-2015
Fondation Sophia Antipolis
2014
Université Paris Cité
2006-2012
In Alzheimer disease (AD), the perturbation of endoplasmic reticulum (ER) calcium (Ca²⁺) homeostasis has been linked to presenilins, catalytic core in γ-secretase complexes cleaving amyloid precursor protein (APP), thereby generating amyloid-β (Aβ) peptides. Here we investigate whether APP contributes ER Ca²⁺ and could turn influence Aβ production. We show that overexpression wild-type human (APP(695)), or harboring Swedish double mutation (APP(swe)) triggers increased ryanodine receptor...
Abstract Several lines of recent evidence indicate that the amyloid precursor protein-derived C-terminal fragments (APP-CTFs) could correspond to an etiological trigger Alzheimer’s disease (AD) pathology. Altered mitochondrial homeostasis is considered early event in AD development. However, specific contribution APP-CTFs structure, function, and mitophagy defects remains be established. Here, we demonstrate neuroblastoma SH-SY5Y cells expressing either APP Swedish mutations, or...
Alteration of mitochondria-associated membranes (MAMs) has been proposed to contribute the pathogenesis Alzheimer's disease (AD).We studied herein subcellular distribution, processing, and protein interactome amyloid- precursor (APP) its proteolytic products in MAMs.We reveal that APP catabolites are present MAMs cellular models overexpressing wild type or harboring double Swedish London familial AD mutations, brains transgenic mice model AD.Furthermore, we evidenced both and ␥secretases...
Anatomical lesions in Alzheimer disease-affected brains mainly consist of senile plaques, inflammation stigmata, and oxidative stress. The nuclear factor-κB (NF-κB) is a stress-activated transcription factor that activated around plaques. We have assessed whether NF-κB could be differentially regulated at physiological or supraphysiological levels amyloid β (Aβ) peptides. Under these experimental conditions, we delineated the putative NF-κB-dependent modulation all cellular participants Aβ...
Deviation of the ambient temperature is one most ubiquitous stimuli that continuously affect mammals' skin. Although role warmth receptors in epidermal homeostasis (EH) was elucidated recent years, mystery keratinocyte mild-cold sensor remains unsolved. Here we report cloning and characterization a new functional isoform transient receptor potential M8 (TRPM8) receptor, dubbed TRPM8 (eTRPM8), which localized endoplasmic reticulum membrane controls mitochondrial Ca(2+) concentration...
Abstract Mitochondria dysfunctions and mitophagy failure have been associated with several Alzheimer’s disease (AD) related molecular actors including amyloid beta (Aβ) recently the precursor protein-C terminal fragments (APP-CTFs). The efficacy of process in neurons relies on regulated mitochondrial transport along axons involving a complex machinery. contribution protein (APP) its derived to machinery alterations AD not investigated before. We report herein change expression proteins (SNPH...
Recent work has shown that Bcl-2 and other anti-apoptotic proteins partially deplete the endoplasmic reticulum (ER) Ca(2+) store this alteration of signaling reduces cellular sensitivity to apoptotic stimuli. We expressed in HeLa cells Bcl-2, Bax, Bcl-2/Bax chimeras which putative pore-forming domains two (alpha 5-alpha 6) were mutually swapped, comparing effects on relating them defined molecular domains. The results showed only ER levels effect does not depend alpha 6 helices oncoprotein....
The hepatitis B virus X protein (HBx) is a multifunctional protein, acting on different targets (e.g. transcription factors, cytoplasmic kinases, and mitochondrial proteins) exerting cellular effects as diverse stimulation of cell proliferation apoptosis. In its biological effects, the modulation Ca2+ signals has been proposed to be involved, but direct assessment homeostasis in HBx-transfected cells not carried out yet. this work, we have employed for purpose aequorin-based recombinant...
The six minichromosome maintenance proteins (Mcm2–7) are required for both the initiation and elongation of chromosomal DNA, ensuring that DNA replication takes place once, only during S phase. Here we report on cloning a new human Mcm gene (hMcm8) characterisation its protein product. hMcm8 contains central domain conserved in Mcm2–7 family, is expressed range cell lines tissues. mRNA accumulates G 1 /S phase, while detectable throughout cycle. Immunoprecipitation‐based studies did not...
Summary. Hepatitis delta virus (HDV) coinfection or superinfection in hepatitis B (HBV)‐infected patients results a more aggressive liver disease, with often fulminant forms and rapid progression to cirrhosis hepatocellular carcinoma. The mechanism(s) for this pejorative evolution remains unclear. To explore specific HDV pathogenesis, we used model of transient transfection plasmids expressing the small (sHDAg p24) large (LHDAg p27) antigen hepatocyte cell lines. We found that production...
BackgroundMitophagy and mitochondrial dynamics alterations are two major hallmarks of neurodegenerative diseases. Dysfunctional mitochondria accumulate in Alzheimer's disease–affected brains by yet unexplained mechanisms.MethodsWe combined cell biology, molecular pharmacological approaches to unravel a novel pathway which presenilins control phosphatase tensin homolog–induced kinase 1 (Pink-1) expression transcription. In vivo were carried out on various transgenic knockout animals as well...