C
Céline Marionneau
Researcher at University of Nantes
Publications - 44
Citations - 2492
Céline Marionneau is an academic researcher from University of Nantes. The author has contributed to research in topics: Phosphorylation & Nav1.5. The author has an hindex of 25, co-authored 42 publications receiving 2250 citations. Previous affiliations of Céline Marionneau include Centre national de la recherche scientifique & Washington University in St. Louis.
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Journal ArticleDOI
Specific pattern of ionic channel gene expression associated with pacemaker activity in the mouse heart
Céline Marionneau,Brigitte Couette,Jie Liu,Huiyu Li,Matteo E. Mangoni,Joël Nargeot,Ming Lei,Denis Escande,Sophie Demolombe +8 more
TL;DR: The present study provides the first genome‐scale regional ionic channel expression profile in the mouse heart by using large‐scale real‐time RT‐PCR and two‐way hierarchical clustering analysis of the 71 genes successfully classified the six pools from the four distinct regions.
Journal ArticleDOI
Mouse model of SCN5A-linked hereditary lenègre's disease : Age-related conduction slowing and myocardial fibrosis
Anne Royer,Toon A.B. van Veen,Sabrina Le Bouter,Céline Marionneau,Violaine Griol-Charhbili,Anne-Laure Leoni,Marja Steenman,Harold V.M. van Rijen,Sophie Demolombe,C. A. Goddard,Christine Richer,Brigitte Escoubet,Thérèse Jarry-Guichard,William H. Colledge,Daniel Gros,Jacques M.T. de Bakker,Andrew A. Grace,Denis Escande,Flavien Charpentier +18 more
TL;DR: This work provides the first demonstration that a monogenic ion channel defect can progressively lead to myocardial structural anomalies, including progressive impairment with aging of atrial and ventricular conduction associated withMyocardial rearrangements and fibrosis.
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RhoA Expression Is Controlled by Nitric Oxide through cGMP-dependent Protein Kinase Activation
TL;DR: In vitro and in vivo results show that NO/PKG signaling positively controls RhoA expression and suggest that the basal release of NO is necessary to maintain RhoB expression and RHoA-dependent functions in vascular smooth muscle cells.
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Dysfunction in ankyrin-B-dependent ion channel and transporter targeting causes human sinus node disease.
Solena Le Scouarnec,Solena Le Scouarnec,Solena Le Scouarnec,Naina Bhasin,Claude Vieyres,Thomas J. Hund,Shane R. Cunha,Olha M. Koval,Céline Marionneau,Céline Marionneau,Céline Marionneau,Biyi Chen,Yuejin Wu,Sophie Demolombe,Sophie Demolombe,Sophie Demolombe,Long-Sheng Song,Hervé Le Marec,Hervé Le Marec,Hervé Le Marec,Vincent Probst,Vincent Probst,Vincent Probst,Jean-Jacques Schott,Jean-Jacques Schott,Jean-Jacques Schott,Mark E. Anderson,Peter J. Mohler +27 more
TL;DR: These findings associate abnormal channel targeting with human SND and highlight the critical role of local membrane organization for sinoatrial node excitability.
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Targeted Deletion of Kv4.2 Eliminates I to,f and Results in Electrical and Molecular Remodeling, With No Evidence of Ventricular Hypertrophy or Myocardial Dysfunction
Weinong Guo,W. Edward Jung,Céline Marionneau,Franck Aimond,Haodong Xu,Kathryn A. Yamada,Thomas Schwarz,Sophie Demolombe,Jeanne M. Nerbonne +8 more
TL;DR: Findings demonstrate not only an essential role for Kv4.2 in the generation of mouse ventricular Ito,f channels but also that the loss of Ita,f per se does not have overt pathophysiological consequences.