Effects of anti‐triadin antibody on Ca2+ release from sarcoplasmic reticulum

FEBS Letters

Antoniu, Bozena¹  Brunschwig, J.-P.²  Kang, Jaw-Jou¹  Caswell, Anthony H.²  Ikemoto, Noriaki¹  Brandt, Neil R.² 

[1] Department of Muscle Research, Boston Biomedical Research Institute, Boston, MA 02114, USA;Department of Pharmacology, University of Miami School of Medicine, Miami, FL 33101, USA

关键词: Triadin;    Excitation-contraction coupling;    Ca2+ release;    Sarcoplasmic reticulum;    DHP;    dihydropyridine;    DIR;    depolarization-induced Ca2+ release;    e-c coupling;    excitation-contraction coupling;    HEPES;    N-2 hydroxyethyl piperzine-N-2 ethanesulfuric acid;    JFP;    junctional foot protein;    mAb;    monoclonal antibody;    MES;    2-(N-morpholino) ethanesulfonic acid;    PMSF;    phenylmethyl sulfonyl fluoride;    SR;    sarcoplasmic reticulum;    TC;    terminal cisternae;    T-tubule;    transverse tubule;   

DOI  :  10.1016/0014-5793(92)80100-U

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown