Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-3-11
pubmed:abstractText
In our previous study, the sphingosine-like immunosuppressant, ISP-1, was found to suppress the proliferation of an interleukin-2-dependent cytotoxic T cell line, CTLL-2, through the inhibition of serine palmitoyltransferase, which catalyzes the committed step of sphingolipid biosynthesis. Analysis of the effect of ISP-1 by flow cytometry revealed that the ISP-1-dependent decrease in cell number was not due to inhibition of the cell cycle progression of CTLL-2 cells but to the induction of apoptosis of the cells. The ISP-1-induced apoptosis was inhibited by the addition of sphingosine (2 microM), suggesting that this ISP-1-induced apoptosis is triggered by the decrease in the intracellular levels of sphingolipids caused by the inhibition of serine palmitoyltransferase. However, another interleukin-2-dependent cell line, F7, which was derived from a mouse pro-B cell line, did not show ISP-1-dependent apoptosis, indicating that the effect of ISP-1 may be specific for a certain type of T cell lineage such as CTLL-2. On the other hand, a high dose of sphingosine (5 microM) by itself induced the apoptosis of CTLL-2 cells. This sphingosine-dependent apoptosis was also observed with F7 cells. These results provide evidence that the intracellular levels of sphingolipids play an important role in the signaling of the escape from and onset of apoptosis of CTLL-2 cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1255-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Dual roles of sphingolipids in signaling of the escape from and onset of apoptosis in a mouse cytotoxic T-cell line, CTLL-2.
pubmed:affiliation
Department of Biological Chemistry, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't