Linked Life Data

7694190

Source:http://linkedlifedata.com/resource/pubmed/id/7694190

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-12-13
pubmed:abstractText
The effects of calphostin A on cytoplasmic calcium levels, receptor-mediated calcium release, and membrane input resistance were measured in neuroblastoma cells. Calphostin A is a lipophilic, light-sensitive perylenequinone that generates singlet oxygen when illuminated. It inhibits the activity of protein kinase C (IC50 = 250 nM), but only in the presence of light. Phorbol esters normally attenuate carbachol-evoked calcium release. This effect was blocked by simultaneous exposure to light and calphostin A (40 nM) for 30 min. At higher doses (0.5-1 microM) calphostin A also approximately doubled the resting calcium level and decreased cell input resistance by 51%. These toxic effects did not occur in the dark or after preincubation with the antioxidant alpha-tocopherol. These data support the hypothesis that the calphostins act by partitioning into the membrane and producing singlet oxygen and endoperoxides which then irreversibly modify protein kinase C and other membrane proteins and lipids.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Membrane toxicity of the protein kinase C inhibitor calphostin A by a free-radical mechanism.
pubmed:affiliation
Department of Biological Sciences, Stanford University, Pacific Grove, CA 93950.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't