Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Maxime Albesa"'
Autor:
Simona Casini, Maxime Albesa, Zizun Wang, Vincent Portero, Daniela Ross-Kaschitza, Jean-Sébastien Rougier, Gerard A. Marchal, Wendy K. Chung, Connie R. Bezzina, Hugues Abriel, Carol Ann Remme
Publikováno v:
International Journal of Molecular Sciences, Vol 20, Iss 20, p 5033 (2019)
Dysfunction of the cardiac sodium channel Nav1.5 (encoded by the SCN5A gene) is associated with arrhythmias and sudden cardiac death. SCN5A mutations associated with long QT syndrome type 3 (LQT3) lead to enhanced late sodium current and consequent a
Externí odkaz:
https://doaj.org/article/303d9d696c274f688ffc404464157d77
Autor:
Jean-Sébastien Rougier, Vincent Portero, Gerard A Marchal, Carol Ann Remme, Zizun Wang, Daniela Ross-Kaschitza, Connie R. Bezzina, Hugues Abriel, Wendy K. Chung, Simona Casini, Maxime Albesa
Publikováno v:
Casini, Simona; Albesa, Maxime; Wang, Zizun; Portero, Vincent; Ross-Kaschitza, Daniela; Rougier, Jean-Sébastien; Marchal, Gerard A; Chung, Wendy K; Bezzina, Connie R; Abriel, Hugues; Remme, Carol Ann (2019). Functional Consequences of the SCN5A-p.Y1977N Mutation within the PY Ubiquitylation Motif: Discrepancy between HEK293 Cells and Transgenic Mice. International journal of molecular sciences, 20(20) Molecular Diversity Preservation International MDPI 10.3390/ijms20205033
International journal of molecular sciences, 20(20):5033. Multidisciplinary Digital Publishing Institute (MDPI)
International Journal of Molecular Sciences, Vol 20, Iss 20, p 5033 (2019)
International Journal of Molecular Sciences
Volume 20
Issue 20
International journal of molecular sciences, 20(20):5033. Multidisciplinary Digital Publishing Institute (MDPI)
International Journal of Molecular Sciences, Vol 20, Iss 20, p 5033 (2019)
International Journal of Molecular Sciences
Volume 20
Issue 20
Dysfunction of the cardiac sodium channel Nav1.5 (encoded by the SCN5A gene) is associated with arrhythmias and sudden cardiac death. SCN5A mutations associated with long QT syndrome type 3 (LQT3) lead to enhanced late sodium current and consequent a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2b16c020094caea5e7d0ce05e5c150d6
https://boris.unibe.ch/138164/1/ijms-20-05033.pdf
https://boris.unibe.ch/138164/1/ijms-20-05033.pdf
Autor:
Ludovic Gillet, Richard Redon, Hugues Abriel, Diana Shy, Maria C. Essers, Arie O. Verkerk, Anneke M. van Mil, Rianne Wolswinkel, Jean-Sébastien Rougier, Ninda Syam, Samuel Rotman, Connie R. Bezzina, Carol Ann Remme, Jakob Ogrodnik, Roos F. Marsman, Maxime Albesa, Julien Barc
Publikováno v:
Circulation
Circulation, 130(2), 147-160. Lippincott Williams and Wilkins
Circulation, 130(2), 147-U96
Circulation, 130(2), 147-160. Lippincott Williams and Wilkins
Circulation, 130(2), 147-U96
Background— Sodium channel Na V 1.5 underlies cardiac excitability and conduction. The last 3 residues of Na V 1.5 (Ser-Ile-Val) constitute a PDZ domain–binding motif that interacts with PDZ proteins such as syntrophins and SAP97 at different loc
Publikováno v:
Journal of molecular and cellular cardiology
The voltage-gated cardiac potassium channel hERG1 (human ether-à-gogo-related gene 1) plays a key role in the repolarization phase of the cardiac action potential (AP). Mutations in its gene, KCNH2, can lead to defects in the biosynthesis and matura
Publikováno v:
The Journal of Biological Chemistry
Neuronal precursor cell-expressed developmentally down-regulated 4 (Nedd4) proteins are ubiquitin ligases, which attach ubiquitin moieties to their target proteins, a post-translational modification that is most commonly associated with protein degra
Autor:
Jakob Ogrodnik, Anne-Flore Zmoos, Elise Balse, Stephan E. Lehnart, Hugues Abriel, Stéphane N. Hatem, Stefan Luther, Alain Coulombe, Philip Bittihn, Said El-Haou, Séverine Petitprez, Nour Raad, Maxime Albesa
Publikováno v:
Circulation Research; Vol 108
Rationale: The cardiac sodium channel Na v 1.5 plays a key role in excitability and conduction. The 3 last residues of Na v 1.5 (Ser-Ile-Val) constitute a PDZ-domain binding motif that interacts with the syntrophin–dystrophin complex. As dystrophin
Autor:
Charles Antzelevitch, Vladimir Kaplan, Alessandra Baumer, Christian Templin, Heinrich Sticht, Thomas F. Lüscher, Hector Barajas-Martinez, Dan Hu, Anita Rauch, Hugues Abriel, Jelena-Rima Ghadri, Maxime Albesa, Jean-Sébastien Rougier, Firat Duru, Colleen Puleo
Publikováno v:
European heart journal
Templin, Christian; Ghadri, Jelena-Rima; Rougier, Jean-Sébastien; Baumer, Alessandra; Kaplan, Vladimir; Albesa, Maxime; Sticht, Heinrich; Rauch, Anita; Puleo, Colleen; Hu, Dan; Barajas-Martinez, Héctor; Antzelevitch, Charles; Lüscher, Thomas F; Abriel, Hugues; Duru, Firat (2011). Identification of a novel loss-of-function calcium channel gene mutation in short QT syndrome (SQTS6). European Heart Journal, 32(9), pp. 1077-88. Oxford: Oxford University Press 10.1093/eurheartj/ehr076
Templin, Christian; Ghadri, Jelena-Rima; Rougier, Jean-Sébastien; Baumer, Alessandra; Kaplan, Vladimir; Albesa, Maxime; Sticht, Heinrich; Rauch, Anita; Puleo, Colleen; Hu, Dan; Barajas-Martinez, Héctor; Antzelevitch, Charles; Lüscher, Thomas F; Abriel, Hugues; Duru, Firat (2011). Identification of a novel loss-of-function calcium channel gene mutation in short QT syndrome (SQTS6). European Heart Journal, 32(9), pp. 1077-88. Oxford: Oxford University Press 10.1093/eurheartj/ehr076
AIMS Short QT syndrome (SQTS) is a genetically determined ion channel disorder which may cause malignant tachyarrhythmias and sudden cardiac death. Thus far mutations in five different genes encoding potassium and calcium channel subunits have been r
Publikováno v:
Journal of Cardiovascular Pharmacology. 56:22-28
Cardiac ion channels play an essential role in the generation of the action potential of cardiomyocytes. Over the past 15 years, a new field of research called channelopathies has emerged; it regroups all diseases caused by ion channel dysfunction. I
Autor:
Wendy K. Chung, C. R. Bezzina, Carol Ann Remme, Vincent Portero, Gerard A Marchal, Maxime Albesa, Simona Casini, Jean-Sébastien Rougier, Hugues Abriel
Publikováno v:
Cardiovascular Research. 114:S68-S68
Autor:
Jean-Sebastien, Rougier, Maxime, Albesa, Ninda, Syam, Guillaume, Halet, Hugues, Abriel, Patricia, Viard
Publikováno v:
Pflügers Archiv European Journal of Physiology
Pflügers Archiv European Journal of Physiology, Springer Verlag, 2015, 467 (9), pp.1-11. ⟨10.1007/s00424-014-1636-6⟩
Rougier, Jean-Sébastien; Albesa, Maxime; Syam, Ninda Ratna Maharani; Halet, Guillaume; Abriel, Hugues; Viard, Patricia (2014). Ubiquitin-specific protease USP2-45 acts as a molecular switch to promote α2δ-1-induced downregulation of Ca v1.2 channels. Pflügers Archiv : European journal of physiology, 467(9), pp. 1919-1929. Springer 10.1007/s00424-014-1636-6
Pflügers Archiv European Journal of Physiology, 2015, 467 (9), pp.1-11. ⟨10.1007/s00424-014-1636-6⟩
Pflugers Archiv
Pflügers Archiv European Journal of Physiology, Springer Verlag, 2015, 467 (9), pp.1-11. ⟨10.1007/s00424-014-1636-6⟩
Rougier, Jean-Sébastien; Albesa, Maxime; Syam, Ninda Ratna Maharani; Halet, Guillaume; Abriel, Hugues; Viard, Patricia (2014). Ubiquitin-specific protease USP2-45 acts as a molecular switch to promote α2δ-1-induced downregulation of Ca v1.2 channels. Pflügers Archiv : European journal of physiology, 467(9), pp. 1919-1929. Springer 10.1007/s00424-014-1636-6
Pflügers Archiv European Journal of Physiology, 2015, 467 (9), pp.1-11. ⟨10.1007/s00424-014-1636-6⟩
Pflugers Archiv
International audience; Availability of voltage-gated calcium channels (Cav) at the plasma membrane is paramount to maintaining the calcium homeostasis of the cell. It is proposed that the ubiquitylation/de-ubiquitylation balance regulates the densit
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ec843fa6ab06ced1cc90e8a67d3bcbaf