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These data for the first time demonstrate that Trisk 95's 200-231 region is responsible for ryanodine receptor activation.
The lncRNA TRDN-AS regulates the balance between cardiac and skeletal isoforms of triadin.
CLIMP-63 (Montrer CKAP4 Protéines) (also known as CKAP4 (Montrer CKAP4 Protéines)), is the partner of triadin, is responsible for this association of triads and microtubules.
The minimal KEKE motif of TRN (Montrer TNPO1 Protéines) involved in the interactions with CSQ2, HRC and RyR2 within the Ca2 (Montrer CA2 Protéines)+ release units of cardiac sarcoplasmic reticulum has been defined.
Three regions in triadin are identified that mediate targeting to the junctional domain of sarcoplasmic reticulum.
in skeletal muscle the disruption of Tdn/CASQ (Montrer CASQ1 Protéines) link has a more profound effect on jSR architecture and myoplasmic Ca(2 (Montrer CA2 Protéines)+) regulation than Jct/CASQ (Montrer CASQ1 Protéines) association.
The triadin-to-calsequestrin ratio is a critical modulator of the sarcoplasmic reticulum Ca(2 (Montrer CA2 Protéines)+) signaling in ventricular myocytes.
Ablation of skeletal muscle triadin impairs FKBP12 (Montrer FKBP1A Protéines)/RyR1 (Montrer RYR1 Protéines) channel interactions essential for maintaining resting cytoplasmic Ca2 (Montrer CA2 Protéines)+.
caveolin 3 (Montrer CAV3 Protéines)-containing membrane domains and the calcium release complex are functionally linked and Trdn is instrumental to the regulation of this interaction, the integrity of which may be crucial for muscle physiology.
Results demonstrate a reduction in muscle strength in triadin knockout mice, indicating that triadin plays an essential role in skeletal muscle function and in skeletal muscle structure.
triadin 1 overexpression triggered time-dependent alterations in SR protein (Montrer RNPS1 Protéines) expression, Ca(2 (Montrer CA2 Protéines)+) homeostasis, and contractility, indicating for the first time an inhibitory function of triadin 1 on SR-Ca(2 (Montrer CA2 Protéines)+) release in vivo.
A compound heterozygous mutation in the triadin gene resulted in a particularly arrhythmogenic phenotype with with cardiac arrest in two siblings.
We describe a new family with cathecholaminergic polymorphic ventricular tachycardia (CPVT) linked to the Triadin gene.
Common variants in TRDN and CALM1 are associated with increased risk of sudden cardiac death in patients with chronic heart failure.
TRDN is a novel underlying genetic basis for recessively inherited Long-QT syndrome.
Data show that triadin (TRDN) is a new gene responsible for an autosomal recessive form of ctecholaminergic polymorphic ventricular tachycardia (CPVT).
The researchers found evidence that TRDN may be a susceptibility or marker gene for IgA nephropathy
Histidine-rich Ca-binding protein may play a key role in the regulation of SR Ca cycling through its direct interactions with SERCA2 (Montrer ATP2A2 Protéines) and triadin, mediating a fine cross talk between SR Ca uptake and release in the heart.
proteasome inhibition led to an accumulation of two new modified forms of triadin-1 that were seen with triadin-1 only when it is not glycosylated on Asn(75).
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.
, junctional sarcoplasmic reticulum glycoprotein
, cardiac triadin
, triadin 1
, triadin 32 kDa (TRISK 32)
, triadin 49 kDa (TRISK 49)
, triadin 95