RGD Reference Report - Trisk 32 regulates IP(3) receptors in rat skeletal myoblasts. - Rat Genome Database

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Trisk 32 regulates IP(3) receptors in rat skeletal myoblasts.

Authors: Olah, T  Fodor, J  Oddoux, S  Ruzsnavszky, O  Marty, I  Csernoch, L 
Citation: Olah T, etal., Pflugers Arch. 2011 Oct;462(4):599-610. doi: 10.1007/s00424-011-1001-y. Epub 2011 Aug 3.
RGD ID: 7327228
Pubmed: PMID:21811790   (View Abstract at PubMed)
DOI: DOI:10.1007/s00424-011-1001-y   (Journal Full-text)

To date, four isoforms of triadins have been identified in rat skeletal muscle. While the function of the 95-kDa isoform in excitation-contraction coupling has been studied in detail, the role of the 32-kDa isoform (Trisk 32) remains elusive. Here, Trisk 32 overexpression was carried out by stable transfection in L6.G8 myoblasts. Co-localization of Trisk 32 and IP(3) receptors (IP(3)R) was demonstrated by immunocytochemistry, and their association was shown by co-immunoprecipitation. Functional effects of Trisk 32 on IP(3)-mediated Ca(2+) release were assessed by measuring changes in [Ca(2+)](i) following the stimulation by bradykinin or vasopressin. The amplitude of the Ca(2+) transients evoked by 20 muM bradykinin was significantly higher in Trisk 32-overexpressing (p < 0.01; 426 +/- 84 nM, n = 27) as compared to control cells (76 +/- 12 nM, n = 23). The difference remained significant (p < 0.02; 217 +/- 41 nM, n = 21, and 97 +/- 29 nM, n = 31, respectively) in the absence of extracellular Ca(2+). Similar observations were made when 0.1 muM vasopressin was used to initiate Ca(2+) release. Possible involvement of the ryanodine receptors (RyR) in these processes was excluded, after functional and biochemical experiments. Furthermore, Trisk 32 overexpression had no effect on store-operated Ca(2+) entry, despite a decrease in the expression of STIM1. These results suggest that neither the increased activity of RyR, nor the amplification of SOCE, is responsible for the differences observed in bradykinin- or vasopressin-evoked Ca(2+) transients; rather, they were due to the enhanced activity of IP(3)R. Thus, Trisk 32 not only co-localizes with, but directly contributes to, the regulation of Ca(2+) release via IP(3)R.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TrdnRatpositive regulation of release of sequestered calcium ion into cytosol  IMP  RGD 

Cellular Component

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TrdnRatsarcoplasmic reticulum  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Trdn  (triadin)


Additional Information