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Ludovic Arandel

Explore the profile of Ludovic Arandel including associated specialties, affiliations and a list of published articles. Areas
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Articles 16
Citations 443
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Recent Articles
1.
Frison-Roche C, Demier C, Cottin S, Laine J, Arandel L, Halliez M, et al.
Brain . 2024 Oct; PMID: 39460437
Muscleblind-like proteins (MBNLs) are a family of RNA-binding proteins that play essential roles in the regulation of RNA metabolism. Beyond their canonical role in RNA regulation, MBNL proteins have emerged...
2.
Arandel L, Matloka M, Klein A, Rau F, Sureau A, Ney M, et al.
Nat Biomed Eng . 2022 Feb; 6(2):207-220. PMID: 35145256
Myotonic dystrophy type 1 (DM1) is an RNA-dominant disease whose pathogenesis stems from the functional loss of muscleblind-like RNA-binding proteins (RBPs), which causes the formation of alternative-splicing defects. The loss...
3.
Muraine L, Bensalah M, Dhiab J, Cordova G, Arandel L, Marhic A, et al.
Hum Gene Ther . 2019 Dec; 31(3-4):233-240. PMID: 31880951
The adeno-associated virus (AAV) vector is an efficient tool for gene delivery in skeletal muscle. AAV-based therapies show promising results for treatment of various genetic disorders, including muscular dystrophy. These...
4.
Klein A, Arandel L, Marie J, Furling D
Methods Mol Biol . 2019 Oct; 2056:203-215. PMID: 31586350
Mutant DMPK transcripts containing expanded CUG repeats (CUGexp) are retained within the nucleus of myotonic dystrophy type 1 (DM1) cells as discrete foci. Nuclear CUGexp-RNA foci that sequester MBNL1 splicing...
5.
Klein A, Varela M, Arandel L, Holland A, Naouar N, Arzumanov A, et al.
J Clin Invest . 2019 Sep; 129(11):4739-4744. PMID: 31479430
Antisense oligonucleotides (ASOs) targeting pathologic RNAs have shown promising therapeutic corrections for many genetic diseases including myotonic dystrophy (DM1). Thus, ASO strategies for DM1 can abolish the toxic RNA gain-of-function...
6.
Azibani F, Brull A, Arandel L, Beuvin M, Nelson I, Jollet A, et al.
Mol Ther Nucleic Acids . 2018 Mar; 10:376-386. PMID: 29499949
We assessed the potential of Lmna-mRNA repair by spliceosome-mediated RNA trans-splicing as a therapeutic approach for LMNA-related congenital muscular dystrophy. This gene therapy strategy leads to reduction of mutated transcript...
7.
Arandel L, Polay Espinoza M, Matloka M, Bazinet A, De Dea Diniz D, Naouar N, et al.
Dis Model Mech . 2017 Feb; 10(4):487-497. PMID: 28188264
Myotonic dystrophy type 1 (DM1) and type 2 (DM2) are autosomal dominant neuromuscular diseases caused by microsatellite expansions and belong to the family of RNA-dominant disorders. Availability of cellular models...
8.
Fougerousse F, Bartoli M, Poupiot J, Arandel L, Durand M, Guerchet N, et al.
Mol Ther . 2017 Feb; 15(1):53-61. PMID: 28182933
α-Sarcoglycanopathy (limb-girdle muscular dystrophy type 2D, LGMD2D) is a recessive muscular disorder caused by deficiency in α-sarcoglycan, a transmembrane protein part of the dystrophin-associated complex. To date, no treatment exists...
9.
Freyermuth F, Rau F, Kokunai Y, Linke T, Sellier C, Nakamori M, et al.
Nat Commun . 2016 Apr; 7:11067. PMID: 27063795
Myotonic dystrophy (DM) is caused by the expression of mutant RNAs containing expanded CUG repeats that sequester muscleblind-like (MBNL) proteins, leading to alternative splicing changes. Cardiac alterations, characterized by conduction...
10.
Rau F, Laine J, Ramanoudjame L, Ferry A, Arandel L, Delalande O, et al.
Nat Commun . 2015 May; 6:7205. PMID: 26018658
Myotonic Dystrophy type 1 (DM1) is a dominant neuromuscular disease caused by nuclear-retained RNAs containing expanded CUG repeats. These toxic RNAs alter the activities of RNA splicing factors resulting in...