|1.||Marks, Andrew R: 45 articles (11/2015 - 01/2002)|
|2.||Wehrens, Xander H T: 43 articles (12/2015 - 05/2003)|
|3.||Chen, S R Wayne: 26 articles (10/2015 - 08/2002)|
|4.||Dirksen, Robert T: 26 articles (01/2015 - 07/2002)|
|5.||Reiken, Steven: 24 articles (11/2015 - 01/2002)|
|6.||Treves, Susan: 23 articles (08/2015 - 01/2003)|
|7.||Jungbluth, Heinz: 23 articles (08/2015 - 06/2002)|
|8.||Ikemoto, Noriaki: 23 articles (12/2012 - 01/2002)|
|9.||Muntoni, Francesco: 21 articles (08/2015 - 10/2004)|
|10.||Lai, F Anthony: 20 articles (11/2015 - 09/2003)|
06/01/2012 - "This specific inhibition of RyR2 could modulate Ca cycling and be useful for the treatment of heart failure. "
05/01/2013 - "Correcting these defects using either genetic manipulation (knock-in) in mice, or specific and novel small molecules ameliorates the RyR2 dysfunction, reducing the progression to heart failure and the incidence of arrhythmias."
09/01/2013 - "For the first time we show that skeletal muscle RyR1 from human heart failure is post-translationally modified, which corroborates previous data from experimental animal studies. "
02/17/2012 - "Our studies revealed remodeling of the transverse tubular system (t-system) and the spatial association of ryanodine receptor (RyR) clusters in a canine model of dyssynchronous heart failure (DHF). "
09/10/2010 - "In this study, we tested the hypothesis that cardiac RyR2 is hyponitrosylated in heart failure, because of nitroso-redox imbalance. "
|2.||Cardiac Arrhythmias (Arrythmia)
04/09/2010 - "In conclusion, CPVT mutation causes defective inter-domain interaction, significant reduction in the ability of CaM binding to the RyR2, spontaneous Ca(2+) leak, and then lethal arrhythmia."
01/01/2010 - "Monophasic action potential recordings demonstrated significantly greater incidences of arrhythmia in RyR2(p/s) and RyR2(s/s) hearts as compared to WTs. "
01/01/2006 - "The knowledge gained from various studies of ryanodine receptors under pathologic conditions might lead to the development of new pharmacological or genetic strategies for the treatment of HF or cardiac arrhythmia. "
11/17/2015 - "The model yields several predictions: 1) [ROS] is produced locally near the RyR2 complex during X-ROS signaling and increases by an order of magnitude more than the global ROS signal during myocyte stretching; 2) X-ROS activation just before the action potential, corresponding to ventricular filling during diastole, increases the magnitude of the Ca(2+) transient; 3) during prolonged stretching, the X-ROS-induced increase in Ca(2+) spark rate is transient, so that long-sustained stretching does not significantly increase sarcoplasmic reticulum Ca(2+) leak; and 4) when the chemical reducing capacity of the cell is decreased, activation of X-ROS signaling increases sarcoplasmic reticulum Ca(2+) leak and contributes to global oxidative stress, thereby increases the possibility of arrhythmia. "
03/15/2015 - "Decreased inward rectifying K+ current and increased ryanodine receptor sensitivity synergistically contribute to sustained focal arrhythmia in the intact rabbit heart."
11/01/2005 - "Given the risk of sudden death and the efficacy of beta blocker therapy, the identification of large numbers of RYR2 mutations thus calls for genetic screening, early diagnosis, and subsequent preventive strategies."
07/17/2002 - "The absence of symptoms and PVA on the stress test in more than one-third of carriers of RyR2 mutations, as well as the lack of PVA inducibility by the EP study, underlies the importance of genetic screening for the early diagnosis of asymptomatic carriers and prevention of sudden death."
12/01/2009 - "Incidence of sudden death was monitored prospectively in heterozygous knock-in mice with mutation R176Q in RyR2 (R176Q/+). "
11/01/2006 - "Understanding the causes of aberrant Ca2+ release via RyR2 may assist in the development of effective treatments for the ventricular arrhythmias that often leads to sudden death in HF and in CPVT."
02/01/2006 - "Identification of novel missense mutations of cardiac ryanodine receptor gene in exercise-induced sudden death at autopsy."
03/01/1994 - "Detection of a novel common mutation in the ryanodine receptor gene in malignant hyperthermia: implications for diagnosis and heterogeneity studies."
02/24/1992 - "In this study we describe the isolation of genomic clones of the 5' region of the porcine ryanodine receptor gene, a candidate for malignant hyperthermia in pigs and humans. "
12/01/2015 - "It is important to identify children who are candidates for ophthalmic surgery who might harbor RYR1 mutations because intraoperative malignant hyperthermia is potentially lethal. "
10/01/2015 - "Several Ryanodine Receptor Type 1 Gene Mutations of p.Arg2508 Are Potential Sources of Malignant Hyperthermia."
05/01/2015 - "Next-generation Sequencing of RYR1 and CACNA1S in Malignant Hyperthermia and Exertional Heat Illness."
|5.||Central Core Myopathy (Central Core Disease)
03/01/2008 - "Additionally, the stress syndrome in pigs, caused by mutations in the porcine RYR1 gene, helped to localize the gene causing malignant hypertermia and Central Core myopathy in humans. "
10/15/2004 - "In this study we report for the first time the functional properties of human myotubes isolated from patients harboring the native RYR1 I4898T and R4893W mutations linked to central core disease. "
01/01/2015 - "Mild Clinical Features and Histopathologically Atypical Cores in Two Korean Families with Central Core Disease Harboring RYR1 Mutations at the C-Terminal Region."
10/18/2014 - "Hot spot mutation in C-terminal of the RYR1 gene can only be identified in patients with central core disease, so we suggest this hot spot gene mutation screening apply to the suspicious patient with central core disease only."
10/18/2014 - "In the family case (Patient 2) of central core disease, the c.14678G>A (p.Arg4893Gln) mutation in 102 extron of RYR1 was identified in three members of the family, which had been reported to be a pathogenic mutation. "
|1.||tacrolimus binding protein 1B
|4.||L-Type Calcium Channels (Dihydropyridine Receptor)
|5.||Tacrolimus Binding Proteins (FKBP)
|7.||NADPH Oxidase (NAD(P)H oxidase)
|8.||Creatine Kinase (Creatine Phosphokinase)
|10.||AICA ribonucleotide (CAIR)
|1.||Artificial Respiration (Mechanical Ventilation)
|2.||Positive-Pressure Respiration (PEEP)