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• W1998474809 abstract "Palytoxin (PTX) induces a cation channel through interaction with Na(+),K(+)-ATPase. It is unclear how this action relates to the enzyme catalytic activity. We examined whether the action of PTX depends on the catalytic domain specific for Na(+),K(+)-ATPase. Wild-type Na(+),K(+)-ATPase alpha-subunit (NNN) or its chimera (NCN), in which the catalytic domain was replaced with that of sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase, was co-expressed with beta-subunit in the yeast Saccharomyces cerevisiae. PTX (0.1-100 nM) increased K(+) efflux in NNN- or NCN-transfected cells to a similar degree but not in non-transfected cells. When ouabain-resistant NNN and NCN were expressed, PTX also increased K(+) efflux. Ouabain inhibited the effect of PTX in NNN or NCN cells but not in ouabain-resistant cells. These data suggest that the channel-forming action of PTX does not depend on the catalytic domain species." @default.
• W1998474809 created "2016-06-24" @default.
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• W1998474809 date "2003-04-29" @default.
• W1998474809 modified "2023-10-14" @default.
• W1998474809 title "Channel induction by palytoxin in yeast cells expressing Na⁺,K⁺‐ATPase or its chimera with sarco/endoplasmic reticulum Ca²⁺‐ATPase" @default.
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• W1998474809 doi "https://doi.org/10.1016/s0014-5793(03)00418-6" @default.
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