Linked Life Data

8694507

Source:http://linkedlifedata.com/resource/pubmed/id/8694507

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3B
pubmed:dateCreated
1996-8-29
pubmed:abstractText
Elevations of phosphomonoesters (PMEs) correlate with increased cell growth or increased cell degradation, and have been shown to occur in human tumors as well as animal tumor models and cell lines. Furthermore, decreased PME levels have been observed in tumor patients who respond to therapy. Therefore, understanding the mechanisms underlying the interactions of intrinsic and extrinsic control of PMEs may assist diagnosis and treatment of tumors at the clinical level. In order to probe the underlying mechanisms controlling PME concentrations, we used cells grown in bioreactors and 31P nuclear magnetic resonance spectroscopy to study the effects of proliferative status and exogenous precursor amines on the PMEs phosphorylcholine (PCho) and phosphorylethanolamine (PEtn). In general, PEtn demonstrated an inverse correlation with cell growth, beginning to rise as the stationary growth phase was approached. PCho, on the other hand, generally decreased during log growth, an effect that was reversed by the addition of exogenous choline. The net effect of these changes was a consistent and dramatically lower PCho/PEtn ratio in stationary cultures compared to actively proliferating cultures.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-7005
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1393-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Phosphomonoester metabolism as a function of cell proliferative status and exogenous precursors.
pubmed:affiliation
Department of Biochemistry, College of Medicine, University of Arizona, Tuscon 85724, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.