WorldCat Identities

Dumonceaux, Julie

Overview
Works: 9 works in 10 publications in 2 languages and 14 library holdings
Roles: Other, Author, Thesis advisor, Opponent
Publication Timeline
.
Most widely held works by Julie Dumonceaux
Viral-mediated expression of desmin mutants to create mouse models of myofibrillar myopathy by Pierre Joanne( )

1 edition published in 2013 in English and held by 2 WorldCat member libraries worldwide

CARACTERISATION ET ANALYSE DES MECANISMES D'ENTREE DU PREMIER VIRUS VIH-1 CD4-INDEPENDANT : M7NDK by JULIE DUMONCEAUX( Book )

2 editions published in 2000 in French and held by 2 WorldCat member libraries worldwide

L'ENTREE DES VIRUS VIH DANS LEURS CELLULES CIBLES S'EFFECTUE EN PLUSIEURS ETAPES DONT L'ORDRE EST PRIMORDIAL : LIAISON DE LA GLYCOPROTEINE D'ENVELOPPE GP120 A LA MOLECULE CD4, INTERACTION AVEC LE CO-RECEPTEUR (CCR5 OU CXCR4) PUIS FUSION DES MEMBRANES CELLULAIRES ET VIRALES. CHACUNE DE CES INTERACTIONS EST ACCOMPAGNEE DE CHANGEMENTS DANS LES GLYCOPROTEINES D'ENVELOPPE VIRALE. SI L'UNE DE CES ETAPES EST MANQUANTE OU SI ELLES NE S'EFFECTUENT PAS DANS CET ORDRE PRECIS, IL N'Y AURA PAS ENTREE VIRALE. NOUS AVONS MIS EN EVIDENCE LE PREMIER ISOLAT VIH-1 (APPELE M7NDK) AYANT UNE ENTREE INDEPENDANTE DE LA MOLECULE CD4. CELUI-CI DERIVE DE L'ISOLAT VIH-1 NDK APRES CULTURE A LONG TERME DANS DES CELLULES T CD4+ LYMPHOCYTAIRE CEM. NOUS AVONS MONTRE QUE 7 MUTATIONS LOCALISEES DANS LES REGIONS C2, V3 ET C3 DE GP120 SONT RESPONSABLES DU TROPISME CD4-INDEPENDANT DU VIRUS M7NDK. CE VIRUS UTILISE CXCR4 COMME UNIQUE RECEPTEUR. NOUS AVONS PAR AILLEURS ISOLE UN SECOND VARIANT DU VIRUS WTNDK, LE VIH-1 M5NDK QUI POSSEDE 5 DES 7 MUTATIONS DU VIRUS M7NDK. CE VIRUS PEUT INFECTER DES CELLULES DE SINGE VERT (COS7) EXPRIMANT CD4, CONTRAIREMENT AU VIRUS PARENTAL WTNDK. CE TROPISME A ETE CORRELE AUX 5 MUTATIONS OBSERVEES DANS LES REGIONS V3 ET C3 DE GP120. LE VIRUS M7NDK EST, LUI AUSSI, CAPABLE D'INFECTER CES CELLULES COS7, QUE CELLES-CI EXPRIMENT OU PAS LA MOLECULE CD4. LE RECEPTEUR UTILISE POUR ENTRER DANS CES CELLULES COS7 EST CXCR4 DE SINGE VERT. CE TRAVAIL A PERMIS DE MONTRER QU'UN VIRUS VIH-1 PEUT DERIVER IN VITRO SANS PRESSION DE SELECTION ET QUE PEU DE MUTATIONS SUFFISENT POUR L'ACQUISITION DE CE PHENOTYPE, CE QUI POSE BIEN EVIDEMMENT LE PROBLEME D'UNE TELLE DERIVE IN VIVO
Necroptosis mediates myofibre death in dystrophin-deficient mice by Jennifer E Morgan( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

Segregation between SMCHD1 mutation, D4Z4 hypomethylation and Facio-Scapulo-Humeral Dystrophy: a case report by Marie-Cécile Gaillard( )

1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide

Publisher Correction: Necroptosis mediates myofibre death in dystrophin-deficient mice by Jennifer E Morgan( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

Thérapie par l'exercice et dystrophie facio-scapulo-humérale : étude contrôlée randomisée de 6 mois d'entraînement à domicile : précédée d'une étude histologique du potentiel régénératif musculaire dans deux modèles distincts de myopathies by Sénakpon Landry Cyrille Bankolé( )

1 edition published in 2014 in French and held by 1 WorldCat member library worldwide

Although it is now accepted that physical activity (PA) is not deleterious in myopathies, including muscular dystrophies, there is very little evidence of relevance in the literature. This thesis has allowed to provide for the first time, confirmed evidence of safety and beneficial effects of exercise therapy in FSHD, through an integrative view of the potential benefits of such programs on functional, biological and quality of life. Two groups were randomly formed: control group (CG: 44 ± 10 years) and trained group (TG: 40 ± 13 years). After 6-month of adapted and home-based training, benefits have been reported particularly in terms of aerobic capacity (VO2pic, PMA), strength (MVC) followed by an increase in cross-sectional area (CSA) of muscle fibers, muscle function (muscle endurance, 6MWT) and fatigue experienced by patients. The lack of muscle damage (HES analysis & plasma CK values) and the strong tendency to improving the quality of life, support the idea that our training program is safe. Muscle biology also shows improvements in the activity of some oxidative enzymes (CS and CK). In short, this home-based mixed training program has allowed to achieve functional, tissue and quality of life improvements, which opens perspectives for application to other types of myopathies
Régulation de la différenciation du muscle strié squelettique par la voie let-7 - E2F5 by Jérémie Kropp( )

1 edition published in 2014 in French and held by 1 WorldCat member library worldwide

Développement d'une stratégie thérapeutique pour la dystrophie facio-scapulo-humérale by Anne-Charlotte Marsollier( )

1 edition published in 2017 in French and held by 1 WorldCat member library worldwide

FacioScapuloHumeral Dystrophy (FSHD) is a rare autosomal dominant neuromuscular disorder. This disease is caused by a loss of epigenetic marks within the D4Z4 macrosatellite located in the subtelomeric region of chromosome 4 leading to chromatin relaxation, aberrant expression of the DUX4 transcription factor and a cascade of gene deregulations. So far, there is no curative treatment for FSHD. The aim of this project was to determine whether or not targeting 3'-end key sequences involved in the polyadenylation of mRNA by antisens oligonucleotides (AOs) can be used as an efficient strategy for DUX4 gene silencing in FSHD. Indeed, cleavage and polyadenylation of the 3'-end of mRNAs are fundamental mechanisms of mRNAs maturation required for nuclear export, stability of the mRNAs and efficient translation and consequently could represent interesting targets for suppression of gene expression for gain of function diseases. For the first time, we demonstrated in vitro that targeting 3'-end key sequences involved in the addition of the poly(A) tail, such as the polyadenylation signal and the cleavage site, leads to an efficient extinction of the mRNA targeted and in particular DUX4. Because AOs have a weak cellular uptake and a rapid clearance in vivo, the sequences of the most promising AOs have been vectorised into an AAV vector under the control of the U7 promoter. The first results that we obtained with a FSHD mouse model treated with these vectors are promising. This innovating strategy appears as a therapeutic option for FSHD
Etude du rôle de dux4 dans la physiopathologie de la dystrophie facio-scapulo-humérale by Maxime Ferreboeuf( )

1 edition published in 2014 in French and held by 1 WorldCat member library worldwide

Facioscapulohumeral muscular dystrophy (FSHD) is inherited in an autosomal dominant pattern and is one of the most common muscular dystrophies (7/100 000). FSHD usually manifests in the second decade of life and includes an asymmetric wasting and weakness of facial, shoulder and arm muscles and is affecting the distal muscles in later stages of the disease. D4Z4 repetitions, which are known to be decreased in FSHD patients, comprise an open reading frame encoding a transcription factor called DUX4 that is only expressed in patients affected by FSHD. My PhD thesis project is aiming to better understanding of the role played by DUX4 in human skeletal muscle in order to elucidate its involvement in the pathophysiology of FSHD. As FSHD is a progressive disease, I studied DUX4 mRNA expression in both primary human fetal muscle cells and in fetal muscle tissue of control subjects and FSHD1 patients. For the first time, we were able to demonstrate DUX4 expression at the fetal stage, and in addition, we showed abnormal expression of various genes that has been reported to be altered in adult FSHD patients. Also, our experiments on fetus and adult FSHD patient cells suggested an equal expression of DUX4 protein. Although DUX4 protein is expressed at a very low level in patients (about 0.5 to 10% of the nuclei), it leads to a strong misexpression of a large number of DUX4 target genes. By performing co-cultures between C2C12 mouse myoblasts and control or FSHD human myoblasts, we demonstrated that expression of toxic DUX4 protein occurs only in a limited number of nuclei in FSHD patient cells. Interestingly, we revealed that the expressed DUX4 protein is able to spread from one nucleus into nearby nuclei within the myotubes and hence transmitting the molecular pathological abnormalities. Our research project will give us new insights into the pathophysiological mechanisms underlying FSHD
 
Audience Level
0
Audience Level
1
  General Special  
Audience level: 0.97 (from 0.92 for CARACTERIS ... to 1.00 for CARACTERIS ...)

Languages