scholarly journals Postmortem Molecular Screening for Cardiac Ryanodine Receptor Type 2 Mutations in Sudden Unexplained Death

2006 ◽  
Vol 70 (11) ◽  
pp. 1402-1406 ◽  
Author(s):  
Hajime Nishio ◽  
Misa Iwata ◽  
Koichi Suzuki
Keyword(s):  
Ryanodine Receptor ◽  
Receptor Type ◽  
Molecular Screening ◽  
Sudden Unexplained Death ◽  
Unexplained Death ◽  
Cardiac Ryanodine Receptor

Junctophilin-2  physically interacts with ryanodine receptor type 2 for peripheral coupling of mouse cardiomyocytes

2020 ◽  
Author(s):  
Tianxia Luo ◽  
Ningning Yan ◽  
Mengru Xu ◽  
Fengjuan Dong ◽  
Qian Liang ◽  
...  
Keyword(s):  
Ryanodine Receptor ◽  
Bioinformatic Analysis ◽  
Cardiac Contraction ◽  
Receptor Type ◽  
Immunofluorescent Staining ◽  
Physical Interaction ◽  
C Terminus ◽  
Confocal Immunofluorescence ◽  
Intracellular Ca

Abstract Background: Ryanodine receptor type 2 (RyR2) mediate Ca 2+ release from the endoplasmic and sarcoplasmic reticulum (ER and SR), which is involved in the peripheral coupling of mouse cardiomyocytes, and thereby plays an important role in cardiac contraction. Junctophilin-2 (JPH2, JP2) is anchored to the plasma membrane (PM) and membranes of the ER and SR, and modulates intracellular Ca 2+ handling through regulation of RyR2. However, the potential RyR2 binding region of JPH2 is poorly understood. Methods: The interaction of JPH2 with RyR2 was studied using LC-MS/MS , bioinformatic analysis,co-immunoprecipitation studies in cardiac SR vesicles. GST-pull down analysis was performed to investigate the physical interaction between RyR2 and JPH2 fragments. Immunofluorescent staining was carried out to determine the colocalization of RyR2 and JPH2 in isolated mouse cardiomyocytes. Ion Optix photometry system was used to measure the levels of intracellular Ca 2+ transients in cardiomyocytes isolated from JPH2 knock down mice. Results: We report that (i) JPH2 interacts with RyR2 and (ii) the C terminus of the JPH2 protein can pull down RyR2 receptors. Confocal immunofluorescence imaging indicated that the majority of JPH2 and RyR2 proteins were colocalized near Z-lines. A decrease in the levels of JPH2 expression reduced the amplitude of Ca 2+ transients in cardiomyocytes. Conclusions: This study suggests that the C terminus domain of JPH2 is required for interactions with RyR2 in the context of peripheral coupling of mouse cardiomyocytes, which provide a molecular mechanism for looking for Ca 2+ - related diseases prevention strategies.

Vesl/Homer proteins regulate ryanodine receptor type 2 function and intracellular calcium signaling

Cell Calcium ◽  
2003 ◽  
Vol 34 (3) ◽  
pp. 261-269 ◽  
Author(s):  
Jens H Westhoff ◽  
Sung-Yong Hwang ◽  
R Scott Duncan ◽  
Fumiko Ozawa ◽  
Pompeo Volpe ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Ryanodine Receptor ◽  
Receptor Type ◽  
Intracellular Calcium Signaling ◽  
Homer Proteins

scholarly journals Ryanodine Receptor Type 2 Is Required for the Development of Pressure Overload-Induced Cardiac Hypertrophy

Hypertension ◽  
2011 ◽  
Vol 58 (6) ◽  
pp. 1099-1110 ◽  
Author(s):  
Yunzeng Zou ◽  
Yanyan Liang ◽  
Hui Gong ◽  
Ning Zhou ◽  
Hong Ma ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Ryanodine Receptor ◽  
Pressure Overload ◽  
Receptor Type

scholarly journals Ryanodine Receptor Type 2 Plays a Role in the Development of Cardiac Fibrosis under Mechanical Stretch Through TGFβ-1

2017 ◽  
Vol 58 (6) ◽  
pp. 957-961 ◽  
Author(s):  
Zhiwen Ding ◽  
Jie Yuan ◽  
Yanyan Liang ◽  
Jian Wu ◽  
Hui Gong ◽  
...  
Keyword(s):  
Ryanodine Receptor ◽  
Cardiac Fibrosis ◽  
Mechanical Stretch ◽  
Receptor Type
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