TRDN

TRDN contributes to the regulation of lumenal Ca2+ release via the sarcoplasmic reticulum calcium release channels RYR1 and RYR2, a key step in triggering skeletal and heart muscle contraction (PubMed:19398037, PubMed:17846166 and PubMed:7721813). TRDN is required for normal organization of the triad junction, where T-tubules and the sarcoplasmic reticulum terminal cisternae are in close contact. It is required for normal skeletal muscle strength. TRDN plays a role in excitation-contraction coupling in the heart and in regulating the rate of heart beats (By similarity).

Full Name

Triadin

Function

Contributes to the regulation of lumenal Ca2+ release via the sarcoplasmic reticulum calcium release channels RYR1 and RYR2, a key step in triggering skeletal and heart muscle contraction. Required for normal organization of the triad junction, where T-tubules and the sarcoplasmic reticulum terminal cisternae are in close contact (By similarity).
Required for normal skeletal muscle strength. Plays a role in excitation-contraction coupling in the heart and in regulating the rate of heart beats.

Biological Process

Biological Process cellular calcium ion homeostasis Source:BHF-UCL
Biological Process cytoplasmic microtubule organization Source:BHF-UCL
Biological Process endoplasmic reticulum membrane organization Source:BHF-UCL
Biological Process establishment of localization in cell Source:Ensembl
Biological Process heart contraction Source:BHF-UCL1 Publication
Biological Process muscle contraction Source:ProtInc1 Publication
Biological Process negative regulation of ryanodine-sensitive calcium-release channel activity Source:BHF-UCL1 Publication
Biological Process positive regulation of cell communication by electrical coupling involved in cardiac conduction Source:BHF-UCL
Biological Process positive regulation of ryanodine-sensitive calcium-release channel activity Source:BHF-UCL
Biological Process regulation of cardiac muscle cell membrane potential Source:BHF-UCL
Biological Process regulation of cell communication by electrical coupling Source:BHF-UCL1 Publication
Biological Process regulation of release of sequestered calcium ion into cytosol Source:BHF-UCL1 Publication
Biological Process regulation of release of sequestered calcium ion into cytosol by sarcoplasmic reticulum Source:BHF-UCL
Biological Process release of sequestered calcium ion into cytosol by sarcoplasmic reticulum Source:BHF-UCL
Biological Process response to bacterium Source:Ensembl

Cellular Location

Cell membrane
Sarcoplasmic reticulum membrane

Involvement in disease

Ventricular tachycardia, catecholaminergic polymorphic, 5, with or without muscle weakness (CPVT5):
An arrhythmogenic disorder characterized by stress-induced, bidirectional ventricular tachycardia that may degenerate into cardiac arrest and cause sudden death. Patients present with recurrent syncope, or sudden death after physical activity or emotional stress. Some patients have muscle weakness. CPVT5 inheritance is autosomal recessive.

Topology

Cytoplasmic: 1-47
Helical: 48-68
Lumenal: 69-729

PTM

Phosphorylated by CaMK2.
N-glycosylated.