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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-8-1
pubmed:abstractText
Palytoxin causes potassium efflux and sodium influx in all investigated animals cells. Much evidence points to the sodium pump (Na+/K(+)-ATPase) as the target of the toxin. A heterologous expression system for mammalian Na+/K(+)-ATPase in the brewers yeast Saccharomyces cerevisiae has been used to test this hypothesis. Yeast cells do not contain endogenous sodium pumps but can be transformed with vectors coding for the alpha and beta subunits of the mammalian sodium pump. We now show that transformed yeast cells expressing both alpha and beta subunits of Na+/K(+)-ATPase are highly sensitive to the toxin, as measured by the loss of intracellular potassium. Palytoxin-induced potassium efflux is completely inhibited by 500 microM ouabain. In contrast, nontransformed yeast cells or cells expressing either the alpha or beta subunits are insensitive to palytoxin. Thus, the alpha/beta heterodimer of the sodium pump is required for the release of potassium induced by palytoxin. The results suggest that palytoxin converts the sodium pump into an open channel, allowing the passage of alkali ions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0026-895X
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1132-6
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Palytoxin induces K+ efflux from yeast cells expressing the mammalian sodium pump.
pubmed:affiliation
Institut für Biochemie und Endokrinologie, Justus-Liebig-Universität Giessen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't