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-cADPR. These results strongly favor a specific action of cADPR on RyR1. The responsiveness of RyR1 appears in adult muscles when RyR3 is lacking.
Fulceri, R., Rossi, R., Bottinelli, R., Conti, A., Intravaia, E., Galione, A., et al. (2001). Ca2+ release induced by cyclic ADP ribose in mice lacking type 3 ryanodine receptor. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 288(3), 697-702 [10.1006/bbrc.2001.5834].
Ca2+ release induced by cyclic ADP ribose in mice lacking type 3 ryanodine receptor
Fulceri, R.;Benedetti, A.;Sorrentino, V.;
2001-01-01
Abstract
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-cADPR. These results strongly favor a specific action of cADPR on RyR1. The responsiveness of RyR1 appears in adult muscles when RyR3 is lacking.
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https://hdl.handle.net/11365/20823
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