Gourdon, Geneviève, 19..-....
![Sudoc [ABES], France](/viaf/images/flags/SUDOC.png "Sudoc [ABES], France")
Genevieve Gourdon researcher
VIAF ID: 188477358 (Personal)
Permalink: http://viaf.org/viaf/188477358
Preferred Forms
4xx's: Alternate Name Forms (1)
Works
| Title | Sources |
|---|---|
| Aberrant splicing and expression of the non muscle myosin heavy-chain gene MYH14 in DM1 muscle tissues |
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| Bases moléculaires des anomalies cérébelleuses congénitales et modélisation de la déficience en N-glycosylation des protéines. |
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| Cloning and characterization of the mouse alpha globin cluster and a new hypervariable marker |
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| CRISPR/Cas9-Induced |
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| CTG repeat instability and size variation timing in DNA repair-deficient mice |
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| Defective satellite cells in congenital myotonic dystrophy |
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| Downregulation of the Glial GLT1 Glutamate Transporter and Purkinje Cell Dysfunction in a Mouse Model of Myotonic Dystrophy. |
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| Dysfonction des cellules oligodendriales et anomalies de la myéline dans un modèle de souris transgénique de la dystrophie myotonique de type 1. |
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| La dystrophie myotonique de Steinert. Trinucléotides CTG et réparation de l'ADN : les liaisons dangereuses |
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| Étude de la fonction des protéines MBNL au cours du développement à l'aide de cellules souches humaines induites à la pluripotence |
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| Etude des mécanismes intervenant dans le contrôle transcriptionnel de l'expression des gènes de globines α humaines |
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| Expanded CTG repeat demarcates a boundary for abnormal CpG methylation in myotonic dystrophy patient tissues |
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| The expansion of 300 CTG repeats in myotonic dystrophy transgenic mice does not induce sensory or motor neuropathy |
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| The flash-small-pool PCR: how to transform blotting and numerous hybridization steps into a simple denatured PCR |
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| Implication of oxidative lesions and base excision repair in the tissue selectivity of the somatic instability of CAG repeats in Huntington’s diseease. |
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| Integrative Cell Type-Specific Multi-Omics Approaches Reveal Impaired Programs of Glial Cell Differentiation in Mouse Culture Models of DM1 |
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| Longitudinal in vivo muscle function analysis of the DMSXL mouse model of myotonic dystrophy type 1 |
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| Maternal germline-specific effect of DNA ligase I on CTG/CAG instability. |
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| Mécanismes du dysfonctionnement cérébral dans la dystrophie myotonique de type 1 : impacte des expansions CTG sur la physiologie neuronale et astrogliale. |
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| Mechanisms involved in the transcriptional regulation of the human alpha globin genes. |
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| Mechanisms of brain dysfunction in myotonic dystrophy type 1 : impact of the CTG expansion on oligodendrocytes and myelin |
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| miR-223-3p and miR-24-3p as novel serum-based biomarkers for myotonic dystrophy type 1 |
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| Misregulation of miR-1 processing is associated with heart defects in myotonic dystrophy |
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| The mouse alpha-globin locus regulatory element. |
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| The mouse mismatch repair protein, MSH3, is a nucleoplasmic protein that aggregates into denser nuclear bodies under conditions of stress. |
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| MSH2-dependent germinal CTG repeat expansions are produced continuously in spermatogonia from DM1 transgenic mice. |
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| Muscleblind-like 2-mediated alternative splicing in the developing brain and dysregulation in myotonic dystrophy |
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| Myotonic Dystrophies: State of the Art of New Therapeutic Developments for the CNS. |
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| Myotonic dystrophy mouse models: towards rational therapy development. |
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| Myotonic dystrophy transgenic mice exhibit pathologic abnormalities in diaphragm neuromuscular junctions and phrenic nerves. |
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| Myotonic Dystrophy type 1. CTG repeat instability and DNA metabolism.. |
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| Non-radioactive detection of trinucleotide repeat size variability. |
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| Of Mice and Men: Advances in the Understanding of Neuromuscular Aspects of Myotonic Dystrophy. |
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| Pathological consequences of CTG expansions on the central nervous system of a mouse model of the myotonic dystrophy of Steinert : molecular, proteomics and cellular approaches. |
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| Pathological modeling of monogenic diseases using human embryonic stem cells : proof of concept applied to myotonic dystrophy type 1. |
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| Progressive skeletal muscle weakness in transgenic mice expressing CTG expansions is associated with the activation of the ubiquitin–proteasome pathway |
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| Recherche translationnelle sur les dystrophies myotoniques : étude de biomarqueurs et mise en place d'un observatoire national pour les essais cliniques |
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| Respiratory failure in a mouse model of myotonic dystrophy does not correlate with the CTG repeat length. |
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| Sense and Antisense DMPK RNA Foci Accumulate in DM1 Tissues during Development |
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| Study of the function of MBNL proteins during development using human induced pluripotent stem cells. |
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| Study of the molecular bases underlying cerebellar defects with emphasis on protein N-glycosylation impairment |
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| Synaptic protein dysregulation in myotonic dystrophy type 1: Disease neuropathogenesis beyond missplicing |
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| Targeting DMPK with Antisense Oligonucleotide Improves Muscle Strength in Myotonic Dystrophy Type 1 Mice |
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| Time-controlled and muscle-specific CRISPR/Cas9-mediated deletion of CTG-repeat expansion in the <i>DMPK</i> gene |
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| Transgenic mice carrying large human genomic sequences with expanded CTG repeat mimic closely the DM CTG repeat intergenerational and somatic instability. |
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| Le triplet CTG instable impliqué dans la dystrophie myotonique de Steinert : un "serial" acteur imprévisible |
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| Triplet-repeat oligonucleotide-mediated reversal of RNA toxicity in myotonic dystrophy. |
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| The unstable CTG trinucleotide repeat, involved in Myotonic Dystrophy an unforeseeable actor. |
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| Unusual association of a unique CAG interruption in 5' of DM1 CTG repeats with intergenerational contractions and low somatic mosaicism |
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| Utilisation d'un modèle drosophile pour l'identification de marqueurs moléculaires responsables des symptômes musculaires et cardiaques de la maladie de Steinert |
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