Linked Life Data

15725661

Source:http://linkedlifedata.com/resource/pubmed/id/15725661

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-2-23
pubmed:abstractText
Recently, we found that vaticanol C (a resveratrol tetramer), which was isolated from stem bark of Dipterocarpaceae, exhibited growth suppression and induction of apoptosis via the loss of mitochondrial membrane potential and consequent caspases activation. The detailed mechanisms are not clearly understood. We decided to attempt to gain further insight into the mechanisms underlying vaticanol C-induced apoptosis in HL-60 cells. Treatment of HL-60 cells with vaticanol C was found to cause a marked decrease in the level of phosphorylated extracellular signal-regulated kinase (ERK) concurrent with inhibited phosphorylation of its upstream kinase mitogen-activates protein kinase kinase (MEK). Moreover, exposure to vaticanol C led to a significant reduction in the level of phosphorylated Akt. Thus, vaticanol C induced inhibition of both ERK and Akt phosphorylation, resulting in reduced phosphorylation of Bad. These results suggest that vaticanol C might induce apoptosis via a mechanism involving activation of Bad through disruption of pro-survival signaling pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0916-8451
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
353-6
pubmed:dateRevised
2006-4-13
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Vaticanol C-induced cell death is associated with inhibition of pro-survival signaling in HL60 human leukemia cell line.
pubmed:affiliation
Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan. kohguchi@giib.or.jp
pubmed:publicationType
Journal Article