Linked Life Data

8062431

Source:http://linkedlifedata.com/resource/pubmed/id/8062431

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-9-20
pubmed:abstractText
We have investigated the mechanism of action of the putative second messenger, cyclic ADP-ribose (cADPR), on the cardiac ryanodine-sensitive Ca(2+)-release channel. Current fluctuations through single Ca(2+)-release channels have been monitored after incorporation into planar phospholipid bilayers. We demonstrate that activation of the channel by cADPR is dependent on activating levels of cytosolic Ca2+ and lifetime analysis indicates that the mechanism of action may be sensitization of the channel to Ca2+. In the absence of ATP, cADPR activates the channel in a concentration-dependent manner in the presence of 10 mumol/L cytosolic Ca2+. However, in the presence of ATP, cADPR tends to decrease open probability, indicating that cADPR may be acting at the adenine nucleotide binding site. In addition, we demonstrate that the precursor of cADPR, beta-NAD+, and the breakdown product, ADP-ribose, also activate the channel. As cADPR will have to compete with much higher concentrations of beta-NAD+, ADP-ribose, and ATP, we suggest that cADPR does not act as a direct endogenous trigger for the opening of the cardiac Ca(2+)-release channel.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
596-600
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Cyclic ADP-ribose competes with ATP for the adenine nucleotide binding site on the cardiac ryanodine receptor Ca(2+)-release channel.
pubmed:affiliation
Department of Cardiac Medicine, National Heart and Lung Institute, University of London, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't