Cav1.2 and Cav1.3 were distributed on cellular membrane and cytoplasm as IP[sub]3R1, IP[sub]3R2, IP[sub]3R3, and RyR2 in both groups, but positive staining of Cav1.2,
IP3R1, IP3R2, and RyR2 were not uniform in achalasia.
For example, antago-miR mediated inactivation of miR-25, which is selectively upregulated in cardiomyocytes from TAC-overloaded hearts and targets mRNAs such as sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) and inositol-3'-phosphate receptor-1 (
IP3R1), improves calcium reuptake and myocardial contractility during HF [175].
After transfer, membranes were immunoblotted with the following primary antibodies: PMCA1, PMCA 4, and PMCA total (Affinity Bioreagents, Rockford, IL), SERCA 2 (Thermo Scientific, Pierce antibodies, Rockford, IL, USA), NCX1 (Swant, Bellinzona, Switzerland), STIM1 (Cell Signaling, Beverly, USA), Orai1 (Proteintech, USA), and
IP3R1 (Millipore, USA).
(2011) Genetic ablation and chemical inhibition of
IP3R1 reduce mutant huntingtin aggregation.
Liu, "TNF[alpha]-induced
IP3R1 expression through TNFR1/PC-PLC/ PKC[alpha] and TNFR2 signalling pathways in human mesangial cell," Nephrology Dialysis Transplantation, vol.
Phosphorylation of
IP3R1 and the regulation of [Ca.sup.2+]i response at fertilization: a role for the MAP kinase pathway.
Mikoshiba and colleagues demonstrated that a neuronal protein called inositol 1,4,5-trisphosphate receptor 1 (
IP3R1) which regulates cellular calcium signaling was destroyed by ER stress and subsequently induced neuronal cell death and brain damage.