Ryanodine Receptor Calcium Release Channel
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Subject Areas on Research
- A SNO storm in skeletal muscle.
- Aberrant S-nitrosylation mediates calcium-triggered ventricular arrhythmia in the intact heart.
- Activation of the cardiac calcium release channel (ryanodine receptor) by poly-S-nitrosylation.
- Altered stored calcium release in skeletal myotubes deficient of triadin and junctin.
- Ankyrin-B is required for intracellular sorting of structurally diverse Ca2+ homeostasis proteins.
- Calcium Signaling and Cardiac Arrhythmias.
- Calcium entry in skeletal muscle.
- Calmodulin and CaMKII as molecular switches for cardiac ion channels.
- Cell penetration properties of maurocalcine, a natural venom peptide active on the intracellular ryanodine receptor.
- Classes of thiols that influence the activity of the skeletal muscle calcium release channel.
- Cysteine-3635 is responsible for skeletal muscle ryanodine receptor modulation by NO.
- De novo mutations in synaptic transmission genes including DNM1 cause epileptic encephalopathies.
- Disrupted junctional membrane complexes and hyperactive ryanodine receptors after acute junctophilin knockdown in mice.
- Dynamic denitrosylation via S-nitrosoglutathione reductase regulates cardiovascular function.
- Enhanced calcium cycling and contractile function in transgenic hearts expressing constitutively active G alpha o* protein.
- Excitation-contraction coupling in airway smooth muscle.
- High-affinity [3H]PN200-110 and [3H]ryanodine binding to rabbit and frog skeletal muscle.
- Homer modulates NFAT-dependent signaling during muscle differentiation.
- Hypoxia reprograms calcium signaling and regulates myoglobin expression.
- Interpreting Incidentally Identified Variants in Genes Associated With Catecholaminergic Polymorphic Ventricular Tachycardia in a Large Cohort of Clinical Whole-Exome Genetic Test Referrals.
- Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms.
- Nitric oxide, NOC-12, and S-nitrosoglutathione modulate the skeletal muscle calcium release channel/ryanodine receptor by different mechanisms. An allosteric function for O2 in S-nitrosylation of the channel.
- Non-sense mutations in the dihydropyridine receptor beta1 gene, CACNB1, paralyze zebrafish relaxed mutants.
- Oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor-Ca2+ release channel by NADPH oxidase 4.
- Oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor/Ca2+ release channel (RyR1): sites and nature of oxidative modification.
- Physiology of nitric oxide in skeletal muscle.
- Purification and reconstitution of the calcium release channel from skeletal muscle.
- RNA-Mediated Reprogramming of Primary Adult Human Dermal Fibroblasts into c-kit(+) Cardiac Progenitor Cells.
- Redox activation of intracellular calcium release channels (ryanodine receptors) in the sustained phase of hypoxia-induced pulmonary vasoconstriction.
- Reduced junctional Na+/Ca2+-exchanger activity contributes to sarcoplasmic reticulum Ca2+ leak in junctophilin-2-deficient mice.
- Regulation of ryanodine receptors by reactive nitrogen species.
- Regulation of the cardiac muscle ryanodine receptor by O(2) tension and S-nitrosoglutathione.
- Regulation of the skeletal muscle ryanodine receptor/Ca2+-release channel RyR1 by S-palmitoylation.
- Ryanodine receptors in muscarinic receptor-mediated bronchoconstriction.
- S-nitrosylation: spectrum and specificity.
- Single-target molecule detection with nonbleaching multicolor optical immunolabels.
- Skeletal muscle sarcoplasmic reticulum contains a NADH-dependent oxidase that generates superoxide.
- Stac3 is a component of the excitation-contraction coupling machinery and mutated in Native American myopathy.
- Structural and functional characterization of the purified cardiac ryanodine receptor-Ca2+ release channel complex.
- The ankyrin-B C-terminal domain determines activity of ankyrin-B/G chimeras in rescue of abnormal inositol 1,4,5-trisphosphate and ryanodine receptor distribution in ankyrin-B (-/-) neonatal cardiomyocytes.
- The skeletal muscle calcium release channel: coupled O2 sensor and NO signaling functions.
- Transgenic overexpression of the Ca2+-binding protein S100A1 in the heart leads to increased in vivo myocardial contractile performance.
- Zebrafish relatively relaxed mutants have a ryanodine receptor defect, show slow swimming and provide a model of multi-minicore disease.
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Keywords of People
- Bennett, Vann, George B. Geller Professor for Research in Molecular Biology in the School of Medicine, Duke Cancer Institute
- Erickson, Harold Paul, James B. Duke Professor of Cell Biology, Biomedical Engineering
- Landstrom, Andrew Paul, Assistant Professor of Pediatrics, Pediatrics, Cardiology
- Pitt, Geoffrey Stuart, Adjunct Professor in the Department of Medicine, Medicine, Cardiology