Linked Life Data

8328990

Source:http://linkedlifedata.com/resource/pubmed/id/8328990

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1993-8-11
pubmed:abstractText
Folate-binding protein (FBP), a high-affinity folate receptor, is responsible for cellular accumulation of folate and folate analogs such as methotrexate in human KB (nasopharyngeal carcinoma) cells. Both FBP and FBP mRNA increase 3- to 5-fold when KB cells are grown in folate-deficient (less than 10 nM folate) medium (KB-FD), compared with growth in standard folate-replete medium containing at least 2 microM folate (KB-FR). The possible mechanisms of enhanced FBP gene expression in KB-FD were examined in this study. Southern blot analysis revealed no significant change in the FBP gene organization or copy number in the KB-FD DNA. While hypomethylation of the FBP gene was observed in KB-FD DNA, relative to KB-FR DNA, exposure of KB-FR to the DNA methylation inhibitors did not result in elevated FBP mRNA levels. The transcriptional rate of the FBP gene was the same in KB-FR and KB-FD. RNA half-life studies indicated that the half-life of FBP mRNA in KB-FD was increased approximately 2.5-fold, compared with KB-FR. Thus, the increase in the steady-state levels of FBP mRNA in KB-FD can be attributed partly to increased FBP mRNA stability.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2537-45
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Altered folate-binding protein mRNA stability in KB cells grown in folate-deficient medium.
pubmed:affiliation
Department of Experimental Therapeutics, Grace Cancer Drug Center, Roswell Park Cancer Institute, Buffalo, NY 14263.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.