Ca2+ release induced by cyclic ADP ribose in mice lacking type 3 ryanodine receptor

被引：6
|
作者：
Fulceri, R
Rossi, R
Bottinelli, R
Conti, A
Intravaia, E
Galione, A
Benedetti, A
Sorrentino, V
Reggiani, C
机构：
[1] Univ Padua, Dept Anat & Physiol, I-35131 Padua, Italy
[2] Univ Oxford, Dept Pharmacol, Oxford OX1 3QT, England
[3] Univ Siena, Dept Neurosci, Mol Med Sect, I-53100 Siena, Italy
[4] Ist Sci San Raffaele, DIBIT, Milan, Italy
[5] Univ Pavia, Inst Human Physiol, I-27100 Pavia, Italy
[6] Univ Siena, Dept Physiopathol & Expt Med, I-53100 Siena, Italy
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 288卷 / 03期
关键词：
skeletal muscles; cADP-ribose; ryanodine receptors; sarcoplasmic reticulum; single muscle fibers;
D O I：
10.1006/bbrc.2001.5834
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The action of cyclic-ADP-ribose was studied on calcium release from sarcoplasmic reticulum of skeletal muscles of neonatal and adult wild-type and RyR3-deficient mice. cADPR increased calcium efflux from microsomes, enhanced caffeine-induced calcium release, and, in 20% of the tests, triggered calcium release in single muscle fibers. These responses occurred only in the diaphragm of adult RyR3-deficient mice. cADPR action was abolished by ryanodine, ruthenium red, and 8-brome-cADPM These results strongly favor a specific action of cADPR on RyR1. The responsiveness of RyR1 appears in adult muscles when RyR3 is lacking. (C) 2001 Academic Press.
引用
收藏
页码：697 / 702
页数：6
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