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Triadin, Trdn, cardiac triadin 1
This gene encodes an integral membrane protein that contains a single transmembrane domain. As similar protein in rabbits plays a role in skeletal muscle excitation-contraction coupling as part of the calcium release complex in association with the ryanodine receptor. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene, and single nucleotide polymorphisms in this gene may be markers for IgA nephritis. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: Calsequestrin, junctin, RyR2, CASQ2, CAN
Papers on Triadin
New Family With Catecholaminergic Polymorphic Ventricular Tachycardia Linked to the Triadin Gene.
Thambo et al., Bordeaux, France. In J Cardiovasc Electrophysiol, Oct 2015
We describe a new family with cathecholaminergic polymorphic ventricular tachycardia (CPVT) linked to the Triadin gene.
Homozygous/Compound Heterozygous Triadin Mutations Associated With Autosomal-Recessive Long-QT Syndrome and Pediatric Sudden Cardiac Arrest: Elucidation of the Triadin Knockout Syndrome.
Ackerman et al., Rochester, United States. In Circulation, Jul 2015
After whole-exome sequencing and variant filtration, a homozygous p.D18fs*13 TRDN-encoded triadin frameshift mutation was discovered in a 10-year-old female patient with LQTS with a QTc of 500 milliseconds who experienced recurrent exertion-induced syncope/cardiac arrest beginning at 1 year of age.
The disorders of the calcium release unit of skeletal muscles: what have we learned from mouse models?
Cancellara et al., Padova, Italy. In J Muscle Res Cell Motil, Feb 2015
The release from the Sarcoplasmic Reticulum stores (SR) is handled by a multiprotein complex called Calcium Release Unit and composed of DiHydroPyridine Receptor or DHPR, Ryanodine Receptor or RYR, Calsequestrin or CASQ, junctin, Triadin, Junctophilin and Mitsugumin 29.
Common Variants in TRDN and CALM1 Are Associated with Risk of Sudden Cardiac Death in Chronic Heart Failure Patients in Chinese Han Population.
Pu et al., Beijing, China. In Plos One, 2014
Moreover, patients carrying G allele of rs361508 on TRDN gene also had increased risk of SCD.
Triadin regulates cardiac muscle couplon structure and microdomain Ca(2+) signalling: a path towards ventricular arrhythmias.
Knollmann et al., Boston, United States. In Cardiovasc Res, 2013
Since the discovery of triadin >20 years ago as one of the major proteins located in the junctional sarcoplasmic reticulum, the field has come a long way in understanding the pivotal role of triadin in orchestrating sarcoplasmic reticulum Ca(2+)-release and hence excitation-contraction (EC) coupling.
[Catecholaminergic polymorphic ventricular tachycardia].
Eckardt et al., Münster, Germany. In Herzschrittmacherther Elektrophysiol, 2012
Mutations of the ryanodine receptor gene (RYR2), the calsequestrin gene (CASQ2), and the triadin gene (TRDN) have been identified as an underlying correlate.
Absence of triadin, a protein of the calcium release complex, is responsible for cardiac arrhythmia with sudden death in human.
Marty et al., Grenoble, France. In Hum Mol Genet, 2012
Data show that triadin (TRDN) is a new gene responsible for an autosomal recessive form of ctecholaminergic polymorphic ventricular tachycardia (CPVT).
Modulation of SR Ca2+ release by the triadin-to-calsequestrin ratio in ventricular myocytes.
Kirchhefer et al., Münster, Germany. In Am J Physiol Heart Circ Physiol, 2012
The triadin-to-calsequestrin ratio is a critical modulator of the sarcoplasmic reticulum Ca(2+) signaling in ventricular myocytes.
Triadin/Junctin double null mouse reveals a differential role for Triadin and Junctin in anchoring CASQ to the jSR and regulating Ca(2+) homeostasis.
Perez et al., Chieti, Italy. In Plos One, 2011
in skeletal muscle the disruption of Tdn/CASQ link has a more profound effect on jSR architecture and myoplasmic Ca(2+) regulation than Jct/CASQ association.
Trisk 32 regulates IP(3) receptors in rat skeletal myoblasts.
Csernoch et al., Debrecen, Hungary. In Pflugers Arch, 2011
findings show that Trisk 32 not only co-localizes with, but directly contributes to, the regulation of Ca(2+) release via IP(3) receptors
On the footsteps of Triadin and its role in skeletal muscle.
Perez, Boston, United States. In World J Biol Chem, 2011
Among these modulators, perhaps one of the most elusive is Triadin, a muscle-specific protein that is involved in many crucial aspect of muscle function.
Etomidate induces cytotoxic effects and gene expression in a murine leukemia macrophage cell line (RAW264.7).
Chung et al., Wuxue, China. In Anticancer Res, 2011
DNA microarray assay indicated that etomidate increased the expression of 17 genes (LOC676175; Gm14636; 2810021G02Rik; Iltifb; Olfr1167; Ttc30b; Olfr766; Gas5; Rgs1; LOC280487; V1rd4; Hist1h2bc; V1rj3; Gm10366; Olfr192; Gm10002 and Cspp1) and reduced the expression of 15 genes: (Gm10152; Gm5334; Olfr216; Lcn9; Gm10683; Gm5100; Tdgf1; Cypt2; Gm5595; 1700018F24Rik; Gm10417; Maml2; Olfr591; Trdn and Apol7c).
Candidate gene expression and intramuscular fat content in pigs.
Guimarães et al., Viçosa, Brazil. In J Anim Breed Genet, 2011
Intramuscular fat (IMF) content in Longissimus dorsi muscle of each animal was extracted and correlated with candidate gene mRNA expression (ATN1, EEF1A2, FABP3, LDLR, MGP, OBSCN, PDHB, TRDN and RYR1).
Ablation of skeletal muscle triadin impairs FKBP12/RyR1 channel interactions essential for maintaining resting cytoplasmic Ca2+.
Perez et al., Boston, United States. In J Biol Chem, 2011
Ablation of skeletal muscle triadin impairs FKBP12/RyR1 channel interactions essential for maintaining resting cytoplasmic Ca2+.
Parallel genotyping of 10,204 single nucleotide polymorphisms to screen for susceptible genes for IgA nephropathy.
Chan et al., Singapore, Singapore. In Ann Acad Med Singapore, 2009
The researchers found evidence that TRDN may be a susceptibility or marker gene for IgA nephropathy
Cell-cell interactions during remodeling of the intestine at metamorphosis in Xenopus laevis.
Brown et al., Baltimore, United States. In Dev Biol, 2009
Transgenic tadpoles expressing a dominant negative TH receptor (TRDN) controlled by epithelial-, fibroblast-, and muscle-specific gene promoters were studied.
Remodeling of insulin producing beta-cells during Xenopus laevis metamorphosis.
Brown et al., Baltimore, United States. In Dev Biol, 2009
Expression of a dominant negative form of the thyroid hormone receptor (TRDN) driven by the elastase promoter not only protects the exocrine pancreas of a transgenic tadpole from TH-induced dedifferentiation but also prevents aggregation of beta-cells at climax.
Catecholaminergic Polymorphic Ventricular Tachycardia
Bloise et al., Seattle, United States. In Unknown Journal, 2004
Mutation in four genes – RYR2, CASQ2, TRDN, and CALM1 – is known to cause CPVT or related phenotypes of adrenergically induced life-threatening arrhythmias.
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