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Titin splicing regulates cardiotoxicity associated with calpain 3 gene therapy for limb-girdle muscular dystrophy type 2A
Lostal W, Roudaut C, Faivre M, et al.
Science translational medicine, 2019, 11, 520
Gamma-Sarcoglycan and Dystrophin Mutation Spectrum in an Algerian Cohort
Dalichaouche I, Sifi Y, Roudaut C, et al.
Muscle & Nerve, 2017, 56, 1, p 129
A comparison of AAV strategies distinguishes overlapping vectors for efficient systemic delivery of the 6.2 kb Dysferlin coding sequence
Pryadkina M, Lostal W, Bourg N, et al.
Molecular therapy. Methods & clinical development, 2015, 2
A new titinopathy: Childhood-juvenile onset Emery-Dreifuss-like phenotype without cardiomyopathy
de Cid R, Ben Yaou R, Roudaut C, et al.
Neurology, 2015, 85, 24, p 2126
Detection of TRIM32 deletions in LGMD patients analyzed by a combined strategy of CGH array and massively parallel sequencing.
Nectoux J, de Cid R, Baulande S, et al.
European journal of human genetics : EJHG, 2014, Epub
CIS-Splicing and Translation of the Pre-Trans-Splicing Molecule Combine with Efficiency in Spliceosome-Mediated RNA Trans-Splicing
Monjaret F, Bourg N, Suel L, et al.
Molecular therapy, 2014, 22, 6, p 1176
Restriction of calpain3 expression to the skeletal muscle prevents cardiac toxicity and corrects pathology in a murine model of limb-girdle muscular dystrophy
Roudaut C, Le Roy F, Suel L, et al.
Circulation, 2013, 128, 10, p. 1094-1104
The phenotype of dysferlin-deficient mice is not rescued by adeno-associated virus-mediated transfer of anoctamin 5
Monjaret F, Suel-Petat L, Bourg-Alibert N, et al.
Human gene therapy. Clinical development, 2013, 24, 2, p. 65-76
Lack of correlation between outcomes of membrane repair assay and correction of dystrophic changes in experimental therapeutic strategy in dysferlinopathy
Lostal W, Bartoli M, Roudaut C, et al.
PLoS ONE, 2012, 7, 5, e38036, 11 p.
Mouse model and therapeutic approach by trans-splicing for TMD and LGMD2J (poster)
Karine C, Daniele N, Florence L, et al.
Congrès : 4th International Congress of Myology, 4ème colloque international de Myologie (9-13 mai 2011; Lille (France))
2011, p. 91
A new pathway encompassing calpain 3 and its newly identified substrate cardiac ankyrin repeat protein is involved in the regulation of the nuclear factor-kappaB pathway in skeletal muscle
Laure L, Daniele N, Suel L, et al.
FEBS journal (The), 2010, 277, 20, p. 4322-4337
Efficient recovery of dysferlin deficiency by dual adeno-associated vector-mediated gene transfer
Lostal W, Bourg N, Roudaut C, et al.
Human molecular genetics, 2010, 19, 10, p. 1897-1907
Removal of the calpain 3 protease reverses the myopathology in a mouse model for titinopathies
Charton K, Daniele N, Vihola A, et al.
Human molecular genetics, 2010, 19, 23, p. 4608-4624
Cardiac ankyrin repeat protein is a marker of skeletal muscle pathological remodelling
Laure L, Suel L, Roudaut C, et al.
FEBS journal (The), 2009, 276, 3, p. 669-684
Cardiac ankyrin repeat protein is a transcriptional marker of both atrophy and dystrophy in skeletal muscles
Laure L, Suel-Petat L, Roudaut C, et al.
Congrès : Congrès international de myologie 2008 (International Congress of Myology 2008; 26-30 mai 2008; Marseille, France)
2008, p. 205
Efficient in vivo dysferlin expression by dual AAV vectors reconstruction
Lostal W, Bourg N, Roudaut C, et al.
Congrès : Congrès international de myologie 2008 (International Congress of Myology 2008; 26-30 mai 2008; Marseille, France)
2008, p. 450
Le facteur de régulation de la transcription Cardiac Ankyrin Repeat Protein est un marqueur du remodelage pathologique du muscle squelettique
Daniele N, Laure L, Suel-Petat L, et al.
Congrès : VIes Journées annuelles de la Société Française de Myologie (SFM) (22-23 octobre 2008; Lausanne (Suisse))
2008, p. 24-25
Partial functionality of a Mini-dysferlin molecule identified in a patient affected with moderately severe primary dysferlinopathy (Poster)
Collectif, Krahn M, Wein N, et al.
Neuromuscular disorders : NMD, 2008, 18, 9-10, p. 781
Partial functionality of a mini-dysferlin molecule identified in a patient affected with moderately severe primary dysferlinopathy
Krahn M, Wein N, Lostal W, et al.
Congrès : Congrès international de myologie 2008 (International Congress of Myology 2008; 26-30 mai 2008; Marseille, France)
2008, p. 444
AAV-mediated delivery of a mutated myostatin propeptide ameliorates calpain 3 but not alpha-sarcoglycan deficiency
Bartoli M, Poupiot J, Vulin A, et al.
Gene therapy, 2007, 14, 9, p. 733-740
A third of LGMD2A biopsies have normal calpain 3 proteolytic activity as determined by an in vitro assay
Milic A, Daniele N, Lochmuller H, et al.
Neuromuscular disorders : NMD, 2007, 17, 2, p. 148-156
Safety and efficacy of AAV-mediated calpain 3 gene transfer in a mouse model of limb-girdle muscular dystrophy type 2A
Bartoli M, Roudaut C, Martin S, et al.
Molecular therapy, 2006, 13, 2, p. 250-259
Looking for factors involved in the specificity of muscle impairment observed in muscular dystrophies (abstract : congrès international de Myologie, 2005)
Duguez S, Roudaut C, Yao R, et al.
Congrès : Congrès international de myologie 2005 (International Congress of Myology 2005; 9-13 mai 2005; Nantes, France)
2005, p. 231
Bidirectional transcriptional activity of the Pgk1 promoter and transmission ratio distortion in Capn3-deficient mice
Taveau M, Stockholm D, Marchand S, et al.
Genomics, 2004, 84, 3, p. 592-595
Calpain 3 is activated through autolysis within the active site and lyses sarcomeric and sarcolemmal components
Taveau M, Bourg N, Sillon G, et al.
Molecular and cellular biology, 2003, 23, 24, p. 9127-9135
