Linked Life Data

7992552

Source:http://linkedlifedata.com/resource/pubmed/id/7992552

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
1995-1-12
pubmed:abstractText
The sodium-dependent transport of anionic amino acids is suppressed in NIH3T3 cells that constitutively express ras oncogenes. In a model of NIH3T3 cells in which ras expression is triggered in the presence of dexamethasone, aspartate transport decreases gradually upon dexamethasone treatment and is almost completely suppressed after two days of incubation in the presence of the steroid. In the same cell model, lovastatin, an inhibitor of beta hydroxy-beta methyl-glutaryl-CoA-reductase and, hence, of farnesylation of p21ras, partially protects aspartate transport from the inhibition observed upon steroid treatment. Determinations of cell glutamate in ras-expressing and non expressing cells indicate that in both cell models glutamate decreases when extracellular medium is depleted of glutamine. However, this decrease is much faster in cells expressing ras (either constitutively or conditionally). It is proposed i) that cell production of oncogenic p21ras hinders sodium-dependent transport of anionic amino acids and ii) that the transport alteration impairs the maintenance of cell levels of glutamate in ras-expressing cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0392-4203
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
147-56
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Anionic amino acid transport in ras- transformed fibroblasts.
pubmed:affiliation
Istituto di Patologia Generale, Università degli Studi di Parma.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't