Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1995-12-7
pubmed:databankReference
pubmed:abstractText
To better understand the accelerated decay of fatty acid synthase (FAS) message that occurs after glucose deprivation (J. Biol. Chem. 1993. 268: 6961-6970), we characterized the 3' terminus of the human message and the kinetics of FAS mRNA decay in HepG2 cells. The FAS gene was localized to human chromosome 17q24-25 and to syntenic distal mouse chromosome 11. Expression of the FAS message in human tissues was ubiquitous with high levels in liver, lung, and intra-abdominal adipose tissue. The 806 nucleotide 3' untranslated region of the human mRNA contained two regions with the instability pentamer AUUUA. Unlike short-lived messages containing AUUUA motifs, FAS mRNA decay after glucose deprivation was not first order, and there were no detectable changes in the poly(A) tail. Glucose deprivation transiently caused FAS message to sediment more rapidly than control message in density gradients. In vivo treatment with different translational inhibitors showed that translation per se was not necessary for FAS mRNA decay; association of polysomes with FAS message protected it from decay. In cell-free decay experiments, FAS mRNA decay was more rapid using components from glucose-deprived than glucose-treated cells. These data suggest that glucose regulates cytoplasmic HepG2 FAS mRNA stability by partitioning the message between a translated pool not subject to degradation and a decay compartment, features reminiscent of regulated stability for other diet-responsive messages.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-2275
pubmed:author
pubmed:issnType
Print
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1507-21
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:7595075-Amino Acid Sequence, pubmed-meshheading:7595075-Animals, pubmed-meshheading:7595075-Base Sequence, pubmed-meshheading:7595075-Carcinoma, Hepatocellular, pubmed-meshheading:7595075-Centrifugation, Density Gradient, pubmed-meshheading:7595075-Chromosome Mapping, pubmed-meshheading:7595075-Chromosomes, Human, Pair 17, pubmed-meshheading:7595075-Fatty Acid Synthetase Complex, pubmed-meshheading:7595075-Glucose, pubmed-meshheading:7595075-Humans, pubmed-meshheading:7595075-Kinetics, pubmed-meshheading:7595075-Liver Neoplasms, pubmed-meshheading:7595075-Mice, pubmed-meshheading:7595075-Molecular Sequence Data, pubmed-meshheading:7595075-RNA, Messenger, pubmed-meshheading:7595075-Rats, pubmed-meshheading:7595075-Ribonuclease H, pubmed-meshheading:7595075-Ribonucleases, pubmed-meshheading:7595075-Sequence Homology, pubmed-meshheading:7595075-Tissue Distribution, pubmed-meshheading:7595075-Tumor Cells, Cultured
pubmed:year
1995
pubmed:articleTitle
Human fatty acid synthase mRNA: tissue distribution, genetic mapping, and kinetics of decay after glucose deprivation.
pubmed:affiliation
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't