Linked Life Data

3262104

Source:http://linkedlifedata.com/resource/pubmed/id/3262104

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
27
pubmed:dateCreated
1988-10-19
pubmed:abstractText
The expression of the gene encoding the facilitated glucose transporter (GT) protein was studied in fibroblast cell lines. Addition of 15% calf serum to confluent BALB/c3T3, NIH3T3, or Rat-2 cells rapidly induced a 5-10-fold increase in GT mRNA, as determined by hybridization of size-fractionated total RNA to a rat brain GT cDNA. The rise in GT mRNA was maximal at 3-4 h after stimulation, and then returned to basal values by 16 h. The serum-stimulated increase in GT mRNA was not blocked by the protein synthesis inhibitors cycloheximide (10 micrograms/ml) or anisomycin (100 microM). In BALB/c3T3 cells, fibroblast growth factor (100 ng/ml), platelet-derived growth factor (5 units/ml), and epidermal growth factor (40 ng/ml) stimulated GT mRNA accumulation, although, when added individually, none of these growth factors increased DNA synthesis. The tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA), which activates the enzyme protein kinase C, also caused GT mRNA accumulation in BALB/c3T3 and NIH3T3 cells. Prolonged pretreatment of cells with TPA abolished the response to TPA but not fibroblast growth factor. The involvement of GT gene transcription was assessed by the nuclear run-on technique. Treatment of NIH3T3 cells with serum increased transcription at least 10-20-fold by 30 min and returned to near basal levels by 2 h. This rapid activation paralleled that of the c-fos gene, but preceded the increase in c-myc gene transcription. These data indicate the following: 1) serum growth factors increase glucose transporter mRNA levels by a process not requiring intermediary new protein synthesis and clearly dissociable from mitogenesis, 2) the changes in GT mRNA are preceded by a rapid and transient activation of GT gene transcription, and 3) there exist protein kinase C-dependent and independent pathways for regulation of GT gene expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
263
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13655-62
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:3262104-Animals, pubmed-meshheading:3262104-Anisomycin, pubmed-meshheading:3262104-Blood, pubmed-meshheading:3262104-Cell Line, pubmed-meshheading:3262104-Cycloheximide, pubmed-meshheading:3262104-DNA, pubmed-meshheading:3262104-Epidermal Growth Factor, pubmed-meshheading:3262104-Fibroblast Growth Factors, pubmed-meshheading:3262104-Gene Expression Regulation, pubmed-meshheading:3262104-Growth Substances, pubmed-meshheading:3262104-Kinetics, pubmed-meshheading:3262104-Mice, pubmed-meshheading:3262104-Monosaccharide Transport Proteins, pubmed-meshheading:3262104-Nucleic Acid Hybridization, pubmed-meshheading:3262104-Platelet-Derived Growth Factor, pubmed-meshheading:3262104-RNA, Messenger, pubmed-meshheading:3262104-Rats, pubmed-meshheading:3262104-Tetradecanoylphorbol Acetate, pubmed-meshheading:3262104-Transcription, Genetic
pubmed:year
1988
pubmed:articleTitle
Growth factors rapidly induce expression of the glucose transporter gene.
pubmed:affiliation
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't