|1.||Dai, Yin: 11 articles (01/2012 - 06/2006)|
|2.||Dai, De-Zai: 10 articles (01/2012 - 01/2006)|
|3.||Wehrens, Xander H T: 6 articles (02/2012 - 05/2003)|
|4.||Rouet-Benzineb, Patricia: 5 articles (01/2013 - 02/2007)|
|5.||Mercadier, Jean-Jacques: 5 articles (01/2013 - 02/2007)|
|6.||Lai, F Anthony: 4 articles (10/2013 - 04/2004)|
|7.||Pezet, Mylène: 4 articles (01/2013 - 04/2008)|
|8.||Chen, S R Wayne: 4 articles (07/2010 - 03/2004)|
|9.||Marks, Andrew R: 4 articles (04/2004 - 05/2003)|
|10.||Gellen, Barnabas: 3 articles (01/2013 - 04/2008)|
06/01/2001 - "Recently, a novel mechanism of cardiac dysfunction in heart failure has been reported on the basis of the following findings:1) PKA hyperphosphorylation of RyR causes a dissociation of FKBP12.6 from RyR, resulting in the abnormal single-channel properties (increased Ca(2+) sensitivity for activation and elevated channel activity associated with destabilization of RyR (Marx et al, Cell 101:365, 2000), 2) a prominent abnormal Ca(2+) leak occurs through RyR, following a partial loss of RyR-bound FKBP12.6 and the resultant conformational change in RyR (Yano M et al, Circulation 102:2131, 2000). "
10/24/2000 - "The level of protein expression of FKBP12.6 was indeed found to be significantly decreased in failing SR. An abnormal Ca(2+) leak through the RyR is present in heart failure, and this leak is presumably caused by a partial loss of RyR-bound FKBP12.6 and the resultant conformational change in RyR. "
01/01/2006 - "A thorough understanding of the structural basis of RyR2-FKBP12.6 interaction should aid in understanding the roles that have been proposed for FKBP12.6 in heart failure and in certain forms of sudden cardiac death."
05/01/2012 - "These findings demonstrate that conditional deletion of CHF1/Hey2 in the myocardium leads to abnormalities in calcium handling mediated by FKBP12.6 that predispose to pressure overload-induced heart failure."
05/01/2012 - "Transcription factor CHF1/Hey2 regulates EC coupling and heart failure in mice through regulation of FKBP12.6."
|2.||Cardiac Arrhythmias (Arrythmia)
09/04/2008 - "CPU0213 is beneficial in treating cardiac insufficiency and preventing cardiac arrhythmias possibly by normalizing hyperphosphorylation of PKCvarepsilon and abnormal FKBP12.6 and SERCA2a. "
08/01/2005 - "Abnormal RyR2, FKBP12.6, SERCA2a, and PLB are also involved in the initiation of cardiac arrhythmias. "
04/09/2004 - "In animals with heart failure and in patients with inherited forms of exercise-induced SCD, depletion of the channel-stabilizing protein calstabin2 (FKBP12.6) from the ryanodine receptor-calcium release channel (RyR2) complex causes an intracellular Ca2+ leak that can trigger fatal cardiac arrhythmias. "
07/01/2010 - "The mechanism by which these mutations cause arrhythmia remains controversial, with discrepant findings related to the role of the RyR2 binding protein FKBP12.6. The purpose of this study was to characterize a novel RyR2 mutation identified in a kindred with clinically diagnosed CPVT. "
08/31/2007 - "Hyperphosphorylation at a single amino acid residue, Ser-2808, has been proposed to directly disrupt the binding of a 12.6-kDa FK506-binding protein (FKBP12.6) to RyR2, causing a RyR2 malfunction that triggers cardiac arrhythmias in human heart failure. "
|3.||Asthma (Bronchial Asthma)
02/01/2014 - "Manipulating the interaction of FKBP12.6 with RyR2 might be a novel and useful treatment for asthma. "
02/01/2014 - "This study examined the interaction of FKBP12.6 with RyR2 in BSMCs in AHR of asthma. "
02/01/2014 - "Dissociation of FKBP12.6 from RyR2 in BSMCs is responsible for the increased calcium response contributing to AHR in asthma. "
02/01/2014 - "The interaction of FKBP12.6 with RyR2 and FKBP12.6 expression was determined in a rat asthma model and in BSMCs treated with inflammatory cytokines. "
01/01/2011 - "Oxidized FKBP12.6 was absent on the SR from PAs pretreated with and without hypoxia, but it was present with a higher amount in the cytosol from PAs pretreated with than without hypoxia. "
01/01/2011 - "Pharmacological and genetic inhibition of intracellular ROS generation prevented hypoxia from decreasing FKBP12.6 on the SR and increasing FKBP12.6 in the cytosol. "
06/15/2012 - "The protein contents were unaffected after hypoxia, tended to increase after ischemia and, for FKBP12.6, a further increase after reperfusion was shown. "
01/01/2011 - "Collectively, we conclude that hypoxia may induce Ca(2+) release by causing ROS-mediated dissociation of FKBP12.6 from RyR2 in PASMCs."
01/01/2011 - "Hypoxia and H(2)O(2) diminished the association of FKBP12.6 from type 2 RyRs (RyR2). "
11/28/2008 - "Increased susceptibility to VF in l-thyroxin-induced cardiomyopathy is related to increase in diastolic Ca(2+) levels, resulting from downregulated FKBP12.6 and upregulated ET system. "
11/28/2008 - "Calcium transients and FKBP12.6 immunohistochemistry were measured by confocal microscopy in isolated cardiomyocytes from cardiomyopathy. "
11/28/2008 - "A decreased mRNA ratio of FKBP12.6 to RyR2 likely reflected dissociation of FKBP12.6 in cardiomyopathy. "
11/28/2008 - "We hypothesized that augmented ventricular fibrillation (VF) on reperfusion of rat cardiomyopathy induced by l-thyroxin may result from elevated diastolic Ca(2+) levels due to dissociation (downregulation) of FKBP12.6 and upregulation of endothelin (ET-1) signaling pathway. "
11/28/2008 - "Downregulated FKBP12.6 expression and upregulated endothelin signaling contribute to elevated diastolic calcium and arrhythmogenesis in rat cardiomyopathy produced by l-thyroxin."
|1.||Ryanodine Receptor Calcium Release Channel (Ryanodine Receptor)
|2.||Tacrolimus Binding Proteins (FKBP)
|6.||Protein Kinase C-epsilon
|7.||NADPH Oxidase (NAD(P)H oxidase)
|8.||1- (methanesulfonamido- 1- naphthyloxy)- 2- (N- (4- methane sulfonamidophenethyl)-N-acetamido)ethane