Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1980-2-28
pubmed:abstractText
To determine if increased 5'-methylthioadenosine phosphorylase activity in activated lymphocytes may be responsible for the decreased inhibitory effect noted when 5'-methylthioadenosine is added after stimulation, the activity of this enzyme was monitored during lymphocyte transformation. A direct correlation existed between the transformation process and 5'-methylthioadenosine phosphorylase activity; the longer the stimulation process progressed, the phosphorylase activity; the longer the stimulation process progressed, the greater the enzyme activity. The 7-deaza analog of 5'-methylthioadenosine, 5'-methylthiotubercidin, was utilized to explore further the role that the phosphorylase may play in the reversal process. 5'-Methylthiotubercidin acted as a potent inhibitor, but not a substrate, of the 5'-methylthioadenosine phosphorylase, and was an even more potent inhibitor of lymphocyte transformation than 5'-methylthioadenosine. However, in direct contrast to the 5'-methylthioadenosine effect, inhibition by 5'-methylthiotubercidin could not be completely reversed. These data suggest the 5'-methylthioadenosine phosphorylase plays an important role in reversing 5'-methylthioadenosine-mediated inhibition and that the potent, nonreversible inhibitory effects of 5'-methylthiotubercidin are due to its resistance to 5'-methylthioadenosine phosphorylase degradation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
588
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
294-301
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1979
pubmed:articleTitle
The role of 5'-methylthioadenosine phosphorylase in 5'-methylthioadenosine-mediated inhibition of lymphocyte transformation.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.