Linked Life Data

18489585

Source:http://linkedlifedata.com/resource/pubmed/id/18489585

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2008-5-23
pubmed:abstractText
The tight junction protein occludin participates in cell adhesion and migration and has been shown to possess antitumorigenic properties; however, the exact mechanism underlying these effects is poorly understood. In liver cell lines, we identified an occludin splice variant deleted in exon 9 (Occ(DeltaE9)). Furthermore, comparison analysis of wild-type occludin (Occ(WT)) and Occ(DeltaE9) revealed that exon 9 played important roles in the induction of mitochondria-mediated apoptosis and the inhibition of invasion, along with the downregulation of matrix metalloproteinase expression. In addition, by using the calcium indicator X-rhod-1, and the inositol trisphosphate receptor inhibitor 2-aminoethoxydiphenyl borate, we found that Occ(WT) but not Occ(DeltaE9) increased calcium release from the endoplasmic reticulum. In conclusion, our results showed that occludin mediates apoptosis and invasion by elevating the cytoplasmic calcium concentration and that exon 9 of occludin is an important region that mediates these effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1742-464X
pubmed:author
pubmed:issnType
Print
pubmed:volume
275
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3145-56
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
A novel splice variant of occludin deleted in exon 9 and its role in cell apoptosis and invasion.
pubmed:affiliation
Department of Biological Sciences and Seoul National University, 56-1 Shillim-dong, Kwanak-gu, Seoul, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't