| Role of lateral amygdala calstabin2 in regulation of fear memory. | Role of lateral amygdala calstabin2 in regulation of fear memory.
Han RW, Liu ZP, Lin HR, Tian AW, Xiao YF, Wei J, Deng KY, Pan BX, Xin HB., Free PMC Article | 02/6/2021 |
| FKBP12.6 plays protective role in cardiac hypertrophy through inhibiting Ca(2+) /calmodulin-mediated signalling pathways. | FKBP12.6 protects heart from AngII-induced hypertrophy through inhibiting Ca(2+) /calmodulin-mediated signalling pathways in vivo and in vitro.
Xiao YF, Zeng ZX, Guan XH, Wang LF, Wang CJ, Shi H, Shou W, Deng KY, Xin HB., Free PMC Article | 12/14/2019 |
| The heart contraction is controlled by the Ca2+-induced Ca2+ release between L-type Ca2+ channels and ryanodine receptors. RyRs became more sensitive to Ca2+ triggers without FKBP12.6, leading to ventricular arrthymias. | Sensitized signalling between L-type Ca2+ channels and ryanodine receptors in the absence or inhibition of FKBP12.6 in cardiomyocytes.
Zhao YT, Guo YB, Gu L, Fan XX, Yang HQ, Chen Z, Zhou P, Yuan Q, Ji GJ, Wang SQ., Free PMC Article | 10/7/2017 |
| Calstabin2 as a key modulator of cardiac aging. | Functional role of Calstabin2 in age-related cardiac alterations.
Yuan Q, Chen Z, Santulli G, Gu L, Yang ZG, Yuan ZQ, Zhao YT, Xin HB, Deng KY, Wang SQ, Ji G., Free PMC Article | 10/10/2015 |
| Sirolimus-FKBP12.6 impairs endothelial barrier function by activation of protein kinase C-alpha and downstream disruption of the p120-VE cadherin interaction in vascular endothelium. | Sirolimus-FKBP12.6 impairs endothelial barrier function through protein kinase C-α activation and disruption of the p120-vascular endothelial cadherin interaction.
Habib A, Karmali V, Polavarapu R, Akahori H, Cheng Q, Pachura K, Kolodgie FD, Finn AV., Free PMC Article | 11/30/2013 |
| genetic approaches confirm the role of FKBP12.6 in regulating cardiac ryanodine receptors | The role of FK506-binding proteins 12 and 12.6 in regulating cardiac function.
Li BY, Chen H, Maruyama M, Zhang W, Zhang J, Pan ZW, Rubart M, Chen PS, Shou W., Free PMC Article | 04/27/2013 |
| the impact of simulated ischemia and reperfusion on expression of the calcium handling proteins FKBP12 and FKBP12.6, and intracellular calcium dynamics was investigated. | Impact of hypoxia, simulated ischemia and reperfusion in HL-1 cells on the expression of FKBP12/FKBP12.6 and intracellular calcium dynamics.
Åström-Olsson K, Li L, Olofsson CS, Borén J, Öhlin H, Grip L. | 09/8/2012 |
| Transcription factor CHF1/Hey2 regulates EC coupling and heart failure in mice through regulation of FKBP12.6. | Transcription factor CHF1/Hey2 regulates EC coupling and heart failure in mice through regulation of FKBP12.6.
Liu Y, Korte FS, Moussavi-Harami F, Yu M, Razumova M, Regnier M, Chin MT., Free PMC Article | 07/7/2012 |
| Cardiac FKBP12.6 overexpression in the mouse blunts pressure overload-induced maladaptive left ventricular remodelling. | Cardiac FKBP12.6 overexpression protects against triggered ventricular tachycardia in pressure overloaded mouse hearts.
Vinet L, Pezet M, Bito V, Briec F, Biesmans L, Rouet-Benzineb P, Gellen B, Prévilon M, Chimenti S, Vilaine JP, Charpentier F, Sipido KR, Mercadier JJ. | 06/12/2012 |
| FKBP12.6 removal enhanced, whereas RyR2 gene deletion blocked the hypoxic increase in Ca(2+)(i) in pulmonary artery smooth muscle cells. | Hypoxia induces intracellular Ca2+ release by causing reactive oxygen species-mediated dissociation of FK506-binding protein 12.6 from ryanodine receptor 2 in pulmonary artery myocytes.
Liao B, Zheng YM, Yadav VR, Korde AS, Wang YX., Free PMC Article | 07/23/2011 |
| Characterize the kinetics of FKBP12/12.6 binding to RyR2 in ventricular myocytes and effects on calcium signaling. | Kinetics of FKBP12.6 binding to ryanodine receptors in permeabilized cardiac myocytes and effects on Ca sparks.
Guo T, Cornea RL, Huke S, Camors E, Yang Y, Picht E, Fruen BR, Bers DM., Free PMC Article | 07/12/2010 |
| FKBP12.6(-/-) mice displayed hyperinsulinemia, & resistance to high fat diet-induced hyperglycemia, suggesting that FKBP12.6 plays an important role in insulin secretion & blood glucose control. | FKBP12.6-knockout mice display hyperinsulinemia and resistance to high-fat diet-induced hyperglycemia.
Chen Z, Li Z, Wei B, Yin W, Xu T, Kotlikoff MI, Ji G., Free PMC Article | 03/1/2010 |
| Dissociation of FKBP12.6 from the RYR2 complex does not play a significant role in beta-adrenergic-stimulated Ca(2+) release in heart cells, whereas this mechanism does underlie the action of cADPR. | Dissociation of FKBP12.6 from ryanodine receptor type 2 is regulated by cyclic ADP-ribose but not beta-adrenergic stimulation in mouse cardiomyocytes.
Zhang X, Tallini YN, Chen Z, Gan L, Wei B, Doran R, Miao L, Xin HB, Kotlikoff MI, Ji G., Free PMC Article | 01/21/2010 |
| The increased vulnerability to AF in FKBP12.6-/- mice substantiates the notion that defective SR Ca(2+) release caused by abnormal RyR2 and FKBP12.6 interactions may contribute to the initiation or maintenance of atrial fibrillation. | Intracellular calcium leak due to FKBP12.6 deficiency in mice facilitates the inducibility of atrial fibrillation.
Sood S, Chelu MG, van Oort RJ, Skapura D, Santonastasi M, Dobrev D, Wehrens XH., Free PMC Article | 01/21/2010 |
| FKBP12.6 plays a role in glucose-induced insulin secretion downstream of ATP production, independently of ATP-sensitive K(+) channels, in pancreatic beta-cells. | FKBP12.6 disruption impairs glucose-induced insulin secretion.
Noguchi N, Yoshikawa T, Ikeda T, Takahashi I, Shervani NJ, Uruno A, Yamauchi A, Nata K, Takasawa S, Okamoto H, Sugawara A. | 01/21/2010 |
| the loss of FKBP12.6 has no significant effect on the conduction and activation of RyR2 or the propensity for spontaneous Ca(2+) release and stress-induced ventricular arrhythmias | Removal of FKBP12.6 does not alter the conductance and activation of the cardiac ryanodine receptor or the susceptibility to stress-induced ventricular arrhythmias.
Xiao J, Tian X, Jones PP, Bolstad J, Kong H, Wang R, Zhang L, Duff HJ, Gillis AM, Fleischer S, Kotlikoff M, Copello JA, Chen SR., Free PMC Article | 01/21/2010 |
| During exercise, RyR2 phosphorylation by protein kinase A dissociates FKBP12.6 from the channel, increasing Ca(2+) release and cardiac contractility. FKBP12.6(-/-) mice showed exercise-induced arrhythmias. | FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function linked to exercise-induced sudden cardiac death.
Wehrens XH, Lehnart SE, Huang F, Vest JA, Reiken SR, Mohler PJ, Sun J, Guatimosim S, Song LS, Rosemblit N, D'Armiento JM, Napolitano C, Memmi M, Priori SG, Lederer WJ, Marks AR. | 01/21/2010 |
| important role of the FKBP12.6/RyR2 complex in stochastic (spontaneous) and receptor-mediated Ca2+ release in smooth muscle. | FKBP12.6 and cADPR regulation of Ca2+ release in smooth muscle cells.
Wang YX, Zheng YM, Mei QB, Wang QS, Collier ML, Fleischer S, Xin HB, Kotlikoff MI. | 01/21/2010 |
| spontaneous, transient outward currents (STOCs) and spontaneous Ca(2+) sparks are altered in FKBP12.6 deficient myocytes relative to wild-type and RYR3 null cells | RYR2 proteins contribute to the formation of Ca(2+) sparks in smooth muscle.
Ji G, Feldman ME, Greene KS, Sorrentino V, Xin HB, Kotlikoff MI., Free PMC Article | 01/21/2010 |
| modulates cardiac excitation-contraction coupling | Oestrogen protects FKBP12.6 null mice from cardiac hypertrophy.
Xin HB, Senbonmatsu T, Cheng DS, Wang YX, Copello JA, Ji GJ, Collier ML, Deng KY, Jeyakumar LH, Magnuson MA, Inagami T, Kotlikoff MI, Fleischer S. | 01/21/2010 |