Genomes and Genes
Gene Symbol: Trdn
Alias: 2310045H21Rik, EG432451, TDN, cardiac triadin
- Triadin deletion induces impaired skeletal muscle functionSarah Oddoux
INSERM U836, Grenoble Institut des Neurosciences, Equipe Muscle et Pathologies, Grenoble F 38000, France
J Biol Chem 284:34918-29. 2009..These results indicate that triadin alteration leads to the development of a myopathy, which could be studied using this new animal model...
- Molecular cloning and characterization of mouse cardiac triadin isoformsC S Hong
Department of Life Science, Kwangju Institute of Science and Technology, 1 Oryong dong, Puk Gu, Kwangju 500 712, South Korea
Gene 278:193-9. 2001..In the present study, mouse cardiac triadin cDNAs have been identified by cDNA library screening and RT-PCR...
- Ablation of skeletal muscle triadin impairs FKBP12/RyR1 channel interactions essential for maintaining resting cytoplasmic Ca2+Jose M Eltit
Department of Anesthesiology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
J Biol Chem 285:38453-62. 2010....
- Caveolin 3 is associated with the calcium release complex and is modified via in vivo triadin modificationStéphane Vassilopoulos
INSERM U836, Grenoble Institut des Neurosciences, Equipe Muscle et Pathologies, Grenoble, France
Biochemistry 49:6130-5. 2010....
- SRp38 regulates alternative splicing and is required for Ca(2+) handling in the embryonic heartYing Feng
Department of Biological Sciences, Columbia University, New York, NY 10027, USA
Dev Cell 16:528-38. 2009..profiles in the SRp38(-/-) embryonic heart revealed a defect in processing of the pre-mRNA encoding cardiac triadin, a protein that functions in regulation of Ca(2+) release from the sarcoplasmic reticulum during excitation-..
- Ablation of triadin causes loss of cardiac Ca2+ release units, impaired excitation-contraction coupling, and cardiac arrhythmiasNagesh Chopra
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 106:7636-41. 2009..Here, we identify the role of triadin using mice with ablation of the Trdn gene (Trdn(-/-))...
- Altered expression of triadin 95 causes parallel changes in localized Ca2+ release events and global Ca2+ signals in skeletal muscle cells in cultureJanos Fodor
Department of Physiology, University of Debrecen, P O Box 22, Hungary
J Physiol 586:5803-18. 2008..These results suggest that Trisk 95 negatively regulates RyR function by suppressing localized calcium release events and global calcium signals in cultured muscle cells...
- Altered stored calcium release in skeletal myotubes deficient of triadin and junctinYing Wang
Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, NC 27599 7260, United States
Cell Calcium 45:29-37. 2009..The results suggest that triadin has a role in facilitating KCl depolarization-induced Ca2+ release in contrast to junctin which has a role in maintaining sarcoplasmic reticulum Ca2+ store size in C2C12 myotubes...
- AAV-mediated intramuscular delivery of myotubularin corrects the myotubular myopathy phenotype in targeted murine muscle and suggests a function in plasma membrane homeostasisAnna Buj-Bello
Department of Neurobiology and Genetics, INSERM U596, CNRS UMR 7104, Universite Louis Pasteur de Strasbourg, College de France, 67404 Illkirch, France
Hum Mol Genet 17:2132-43. 2008..This study provides a proof-of-principle that local delivery of an AAV vector expressing myotubularin can improve the motor capacities of XLMTM muscle and represents a novel approach to study myotubularin function in skeletal muscle...
- Triadins modulate intracellular Ca(2+) homeostasis but are not essential for excitation-contraction coupling in skeletal muscleXiaohua Shen
Department of Anesthesiology, Brigham and Women s Hospital, Boston, MA 02115, USA
J Biol Chem 282:37864-74. 2007..Overall, our data support an indirect role for triadin in regulating myoplasmic Ca(2+) homeostasis and organizing the molecular complex of the triad but not in regulating skeletal-type excitation-contraction coupling...
- Triadin is a critical determinant of cellular Ca cycling and contractility in the heartUwe Kirchhefer
Institut fur Pharmakologie und Toxikologie, Universitatsklinikum Munster, Munster, Germany
Am J Physiol Heart Circ Physiol 293:H3165-74. 2007..Thus the maintenance of triadin expression is essential for normal SR Ca cycling and contractile function...
- Histidine-rich Ca-binding protein interacts with sarcoplasmic reticulum Ca-ATPaseDemetrios A Arvanitis
Molecular Biology Division, Center for Basic Research, Foundation for Biomedical Research of the Academy of Athens, Athens, Greece
Am J Physiol Heart Circ Physiol 293:H1581-9. 2007..Collectively, our data suggest that HRC may play a key role in the regulation of SR Ca cycling through its direct interactions with SERCA2 and triadin, mediating a fine cross talk between SR Ca uptake and release in the heart...
- Stress and high heart rate provoke ventricular tachycardia in mice expressing triadinPaulus Kirchhof
Department of Cardiology and Angiology, Hospital of the University of Münster, Germany
J Mol Cell Cardiol 42:962-71. 2007..An imbalance between prolonged intracellular calcium release and shortening of the ventricular action potential may contribute to genesis of arrhythmias in this model...
- Complementary DNA cloning, genomic characterization and expression analysis of a mammalian gene encoding histidine-rich calcium binding proteinSunghee Hong
Department of Life Science, Gwangju Institute of Science and Technology, Gwangju 500 712, Republic of Korea
Biochim Biophys Acta 1727:188-96. 2005..Collectively, our study provides comprehensive information about the structure and expression of the mammalian HRC gene, together with the comparative expression data of the related SR genes...
- Altered function in atrium of transgenic mice overexpressing triadin 1Uwe Kirchhefer
Institut fur Pharmakologie und Toxikologie, Westfalische Wilhelms Universitat, 48149 Munster, Germany
Am J Physiol Heart Circ Physiol 283:H1334-43. 2002..of SR proteins and contractility in atria of 3-, 6-, and 18-wk-old transgenic mice overexpressing canine cardiac triadin 1 under control of the alpha-myosin heavy chain (MHC) promoter...
- Increased muscle stress-sensitivity induced by selenoprotein N inactivation in mouse: a mammalian model for SEPN1-related myopathyMathieu Rederstorff
Architecture et Reactivite de l ARN, Universite de Strasbourg, CNRS, IBMC, Strasbourg, France
PLoS ONE 6:e23094. 2011....