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Triadin
Surface Glycoproteomic Analysis of Hepatocellular Carcinoma Cells by Affinity Enrichment and Mass Spectrometric Identification
Microarchitecture of the Dyad
Absence of Triadin, a Protein of the Calcium Release Complex, Is Responsible for Cardiac Arrhythmia with Sudden Death in Human
Triadin, a Linker for Calsequestrin and the Ryanodine Receptor
Dual Copy Number Variants Involving 16P11 and 6Q22 in a Case
Generation of a Triadin Knockout Syndrome Zebrafish Model
Molecular Genetics of Exercise-Induced
Structure and Function of the Human Ryanodine Receptors and Their Association with Myopathies—Present State, Challenges, and Perspectives
An Expanded Proteome of Cardiac T-Tubules☆
Investigating the Effect of Chronic Activation of AMP-Activated Protein
The Role of Calsequestrin, Triadin, and Junctin in Conferring Cardiac Ryanodine Receptor Responsiveness to Luminal Calcium
Ablation of Triadin Causes Loss of Cardiac Ca Release Units, Impaired
Calsequestrin Interacts Directly with the Cardiac Ryanodine Receptor Luminal Domain Ahmed Handhle1,2,*, Chloe E
Ryanodine Receptors: Structure, Expression, Molecular Details, and Function in Calcium Release
Triadin (L-20): Sc-33390
Triadin Mutations - a Cause of Ventricular Arrhythmias in Children and Young Adults Jules C
Calsequestrin: a Well-Known but Curious Protein in Skeletal Muscle Jin Seok Woo 1, Seung Yeon Jeong2,3,Jiheepark2,3,Junheechoi2,3 and Eun Hui Lee2,3
Calsequestrin Distribution, Structure and Function, Its Role in Normal and Pathological Situations and the Effect of Thyroid Hormones
Top View
Triadin/Junctin Double Null Mouse Reveals a Differential Role for Triadin and Junctin in Anchoring CASQ to the Jsr and Regulating Ca2+ Homeostasis
NIH Public Access Author Manuscript Cell Calcium
Metabolic Adaptation of White Adipose Tissue to Nutritional and Environmental Challenges
Triadin Binding to the C-Terminal Luminal Loop of the Ryanodine Receptor Is Important for Skeletal Muscle Excitation Contraction Coupling
Absence of Triadin, a Protein of the Calcium Release Complex, Is Responsible for Cardiac Arrhythmia with Sudden Death in Human
Ablation of Triadin Causes Loss of Cardiac Ca Release Units, Impaired
Triadin Is Primarily Confined to the Junctional Sarcoplasmic Reticulum of Mammalian Cardiac Myofibers
Pure Interstitial Dup(6)(Q22.31Q22.31) Ł a Case Report
Altered Skeletal Muscle Mitochondrial Proteome As the Basis of Disruption of Mitochondrial Function in Diabetic Mice Piotr Zabie
Absence of Triadin, a Protein of the Calcium Release Complex, Is Responsible for Cardiac Arrhythmia with Sudden Death in Human
Assessment of the Swine Protein-Annotated Oligonucleotide Microarray Juan Pedro Steibel Michigan State University
Regulation of Ca2+ Signaling in Transgenic Mouse Cardiac Myocytes Overexpressing Calsequestrin
Supplementary Table 1. a Full List of Cancer Genes
Linkage of Familial Dilated Cardiomyopathy with Conduction Defect and Muscular Dystrophy to Chromosome 6Q23 David N
Linkage and Association Studies of Joint Morbidity from Rheumatoid Arthritis JIN-YOUNG MIN, KYOUNG-BOK MIN, JOOHON SUNG, and SUNG-IL CHO
Calsequestrin Interacts Directly with the Cardiac Ryanodine Receptor Luminal Domain