A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum.

A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. Abstract Text:

H Morii,H Takisawa,T Yamamoto,

The Ca2+-induced Ca2+ release channel in the heavy fraction of the sarcoplasmic reticulum (SR) from rabbit skeletal muscle is inactivated during ATP-dependent Ca2+ uptake (Morii, H., Takisawa, H., & Yamamoto, T. (1985) J. Biol. Chem. 260, 11536-11541). AMP, one of the adenine nucleotides which activate the Ca2+ release, delayed the onset of the channel inactivation when added early during the course of the Ca2+ uptake. However, AMP could no longer activate the channel but accelerated the inactivation when added during the later phase of the Ca2+ uptake. In SR passively loaded with Ca2+, the Ca2+ channel which had been activated by AMP and Ca2+ was not spontaneously inactivated. Similarly, during GTP-dependent Ca2+ uptake, the channel activated by AMP was not inactivated. In addition acid phosphatase markedly delayed the onset of the inactivation during ATP-dependent Ca2+ uptake, without affecting Ca2+ ATPase activity or GTP-dependent Ca2+ uptake by heavy SR. The effect of the phosphatase was completely blocked by ruthenium red, a potent inhibitor of the channel. These results suggest that the channel is inactivated through an ATP-dependent process, presumably phosphorylation of proteins in the SR membrane. This was supported by the findings that the reactivation of the inactivated channel by added Ca2+ was markedly accelerated by the addition of acid phosphatase and that several proteins of heavy SR were phosphorylated during ATP-dependent Ca2+ uptake.

A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. Publishing Authors By Initials

H Morii,H Takisawa,T Yamamoto,

For similar musculoskeletal system: muscles: muscle, skeletal: sarcoplasmic reticulum research abstracts see: musculoskeletal system: muscles: muscle, skeletal: sarcoplasmic reticulum research

PUBMED ID PMID:

MEDLINE DATE:

A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of biochemistry

VOLUME: 102

Page Numbers: 263-71

Journal Abbreviation: J. Biochem.

ISSN: 0021-924X

DAY: 19

MONTH: Aug

YEAR: 1987

A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 376600

A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. Keywords Mesh Terms:

KEYWORDS: Sarcoplasmic Reticulum

MESH TERMS: metabolism

Chemical & Substance for Abstract: A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. Information

Substance Name: Calcium-Transporting ATPases

Registry Number: EC 3.6.1.8

Grant and Affiliation Information for A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum.

AFFILIATION: Department of Biology, Faculty of Science, Osaka University.

Country: JAPAN

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: J Biochem

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

A possible role of protein phosphorylation in the inactivation of a Ca2+-induced Ca2+ release channel from skeletal muscle sarcoplasmic reticulum Related Publications

• CO2-enhanced sonographically guided radiofrequency ablation and transcatheter arterial chemoembolization for small hepatocellular carcinoma poorly defined on conventional sonography.
• Contested dominance modifies the anovulatory consequences of social subordination in female marmosets.
• Decreased fractal correlation in diurnal physical activity in chronic fatigue syndrome.
• Descriptive study of gallbladder, extrahepatic bile duct, and ampullary cancers in the United States, 1997-2002.
• Diastereo- and enantioselective synthesis of nitroso Diels-Alder-type bicycloketones using dienamine: mechanistic insight into sequential nitroso Aldol/Michael reaction and application for optically pure 1-amino-3,4-diol synthesis.
• Drosophila CTLA-2-like protein (D/CTLA-2) inhibits cysteine proteinase 1 (CP1), a cathepsin L-like enzyme.
• Dynamic changes in vesicular glutamate transporter 1 function and expression related to methamphetamine-induced glutamate release.
• Effects of bilateral jugular vein ligation on local cerebral blood flow.
• Effects of brain lesions on taste-potentiated odor aversion in rats.
• Effects of chronic unpredictable stress and methamphetamine on hippocampal glutamate function.
• Evaluation of osteogenic/chondrogenic cellular proliferation and differentiation in the xenogeneic periosteal graft.
• Gene expression signatures that can discriminate oral leukoplakia subtypes and squamous cell carcinoma.
• Haloperidol treatment after high-dose methamphetamine administration is excitotoxic to GABA cells in the substantia nigra pars reticulata.
• Imaging of Regional Differences of Muscle Oxygenation during Exercise Using Spatially Resolved NIRS.
• Interactions between methamphetamine and environmental stress: role of oxidative stress, glutamate and mitochondrial dysfunction.
• Intraoperative electro-oculographic Monitoring for Skull Base Surgery.
• Involvement of the Mesolimbic System in Palatability-induced Ingestion.
• Ketamine and N-acetylaspartylglutamate peptidase inhibitor exert analgesia in bone cancer pain.
• Kinetic mechanism of the fastest motor protein, Chara myosin.
• Loss of the TOR kinase Tor2 mimics nitrogen starvation and activates the sexual development pathway in fission yeast.
• Menatetrenone, a vitamin K2 analogue, inhibits hepatocellular carcinoma cell growth by suppressing cyclin D1 expression through inhibition of nuclear factor kappaB activation.
• Myostatin modulates adipogenesis to generate adipocytes with favorable metabolic effects.
• Negative regulation of BMP/Smad signaling by Tob in osteoblasts.
• Prior exposure to chronic stress and MDMA potentiates mesoaccumbens dopamine release mediated by the 5-HT(1B) receptor.
• Regulation of Wnt signalling by receptor-mediated endocytosis.
• Simultaneous gene transfer of bone morphogenetic protein (BMP) -2 and BMP-7 by in vivo electroporation induces rapid bone formation and BMP-4 expression.
• The Role of Orexigenic Neuropeptides in the Ingestion of Sweet-tasting Substances in Rats.
• The relationship between cerebral blood flow and cognitive function in patients with brain insult of various etiology.
• The use of polylactic acid/polyglycolic acid copolymer and gelatin sponge complex containing human recombinant bone morphogenetic protein-2 following condylectomy in rabbits.
• Trehalose Sensitivity of the Gustatory Receptor Neurons Expressing Wild-type, Mutant and Ectopic Gr5a in Drosophila.