The inhibition of the slow phase of depolarization-induced Ca2+ release by an anti-triadin antibody suggests that triadin may be involved in the functional coupling between the DHP receptor and the SR Ca2+ channel.
Implicates triadin in excitation-contraction coupling; leaves open therapeutic targeting pending human validation.
The monoclonal antibody, mAb GE 4.90, raised against triadin, a 95 kDa protein of sarcoplasmic reticulum (SR), inhibits the slow phase of Ca2+ release from SR following depolarization of the T-tubule moiety of the triad. The antibody has virtually no effect on the fast phase of depolarization-induced Ca2+ release nor on caffeine-induced Ca2+ release. Since the slow phase of depolarization-induced Ca2+ release is also inhibited by dihydropyridines (DHP), these results suggest that triadin may be involved in the functional coupling between the DHP receptor and the SR Ca2+ channel.
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Brandt et al. (1992) studied this question.
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