Long QT Syndrome–Associated Mutations in KCNQ1 and KCNE1 Subunits Disrupt Normal Endosomal Recycling of IKs Channels
暂无分享,去创建一个
A. Pfeufer | M. Sanguinetti | B. Attali | F. Lang | J. Tavaré | C. Bucci | G. Seebohm | S. Kääb | U. Hoppe | N. Strutz‐Seebohm | A. Mack | J. Mérot | O. Ureche | U. Henrion | Ravshan Baltaev | Ganna Korniychuk | Katja Steinke | D. Tapken | J. Mérot
[1] R. Kass,et al. IKs response to protein kinase A-dependent KCNQ1 phosphorylation requires direct interaction with microtubules. , 2008, Cardiovascular research.
[2] A. Pfeufer,et al. Regulation of Endocytic Recycling of KCNQ1/KCNE1 Potassium Channels , 2007, Circulation research.
[3] Isabelle Baró,et al. The N-Terminal Juxtamembranous Domain of KCNQ1 Is Critical for Channel Surface Expression: Implications in the Romano-Ward LQT1 Syndrome , 2006, Circulation research.
[4] P. Schraeder,et al. Stress and sudden death , 2006, Epilepsy & Behavior.
[5] Peter Novick,et al. Rabs and their effectors: Achieving specificity in membrane traffic , 2006, Proceedings of the National Academy of Sciences.
[6] Frank Sachse,et al. De novo KCNQ1 mutation responsible for atrial fibrillation and short QT syndrome in utero. , 2005, Cardiovascular research.
[7] S. Pfeffer. Structural Clues to Rab GTPase Functional Diversity* , 2005, Journal of Biological Chemistry.
[8] S. Olesen,et al. Basolateral localisation of KCNQ1 potassium channels in MDCK cells: molecular identification of an N-terminal targeting motif , 2004, Journal of Cell Science.
[9] D. Roden,et al. A Structural Requirement for Processing the Cardiac K+ Channel KCNQ1* , 2004, Journal of Biological Chemistry.
[10] S. V. van IJzendoorn,et al. The subapical compartment: a traffic center in membrane polarity development , 2004, Journal of Cell Science.
[11] A. Busjahn,et al. Association of the Serum and Glucocorticoid Regulated Kinase (sgk1) Gene with QT Interval , 2004, Cellular Physiology and Biochemistry.
[12] J. Cherfils,et al. The Structural GDP/GTP Cycle of Rab11 Reveals a Novel Interface Involved in the Dynamics of Recycling Endosomes* , 2004, Journal of Biological Chemistry.
[13] F. Maxfield,et al. Endocytic recycling , 2004, Nature Reviews Molecular Cell Biology.
[14] R. Prekeris. Rabs, Rips, FIPs, and Endocytic Membrane Traffic , 2003, TheScientificWorldJournal.
[15] Ying Wang,et al. KCNQ1 gain-of-function mutation in familial atrial fibrillation. , 2003, Science.
[16] R. Pagano,et al. Glycosphingolipids Internalized via Caveolar-related Endocytosis Rapidly Merge with the Clathrin Pathway in Early Endosomes and Form Microdomains for Recycling* , 2003, The Journal of Biological Chemistry.
[17] F. Lang,et al. Regulation of Channels by the Serum and Glucocorticoid-Inducible Kinase - Implications for Transport, Excitability and Cell Proliferation , 2003, Cellular Physiology and Biochemistry.
[18] R. Pagano,et al. Endocytosis and sorting of glycosphingolipids in sphingolipid storage disease. , 2002, Trends in cell biology.
[19] V. Puri,et al. Rab proteins mediate Golgi transport of caveola-internalized glycosphingolipids and correct lipid trafficking in Niemann-Pick C cells. , 2002, The Journal of clinical investigation.
[20] Junko Kurokawa,et al. Requirement of a Macromolecular Signaling Complex for β Adrenergic Receptor Modulation of the KCNQ1-KCNE1 Potassium Channel , 2002, Science.
[21] F. Lang,et al. Regulation of KCNE1-dependent K+ current by the serum and glucocorticoid-inducible kinase (SGK) isoforms , 2002, Pflügers Archiv.
[22] P. Cohen,et al. Regulation and Physiological Roles of Serum- and Glucocorticoid-Induced Protein Kinase Isoforms , 2001, Science's STKE.
[23] M. Bang,et al. Specific interaction of the potassium channel beta-subunit minK with the sarcomeric protein T-cap suggests a T-tubule-myofibril linking system. , 2001, Journal of molecular biology.
[24] M. Viitasalo,et al. Response of the QT interval to mental and physical stress in types LQT1 and LQT2 of the long QT syndrome , 2001, Heart.
[25] J. Towbin,et al. Genotype and severity of long QT syndrome. , 2001, Drug metabolism and disposition: the biological fate of chemicals.
[26] A. Kessler,et al. Rab11 is associated with GLUT4-containing vesicles and redistributes in response to insulin , 2000, Diabetologia.
[27] M. Sanguinetti,et al. Mutations in the hminK gene cause long QT syndrome and suppress lKs function , 1997, Nature Genetics.
[28] F. Lang,et al. Cloning and characterization of a putative human serine/threonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[29] Jacques Barhanin,et al. KvLQT1 and IsK (minK) proteins associate to form the IKS cardiac potassium current , 1996, Nature.
[30] M. Sanguinetti,et al. Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel. , 1996, Nature.
[31] J. Born,et al. Hormonal secretion during nighttime sleep indicating stress of daytime exercise. , 1995, Journal of applied physiology.
[32] M. Zerial,et al. Membrane association of Rab5 mediated by GDP-dissociation inhibitor and accompanied by GDP/GTP exchange , 1994, Nature.
[33] A. Moss,et al. Stress and sudden death. The case of the long QT syndrome. , 1991, Circulation.
[34] R. S. Eliot,et al. Role of emotions and stress in the genesis of sudden death. , 1985, Journal of the American College of Cardiology.