Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1992-3-10
pubmed:abstractText
Rat insulin-like growth factor-I (IGF-I) mRNAs with different 5'-untranslated region/prepeptide coding sequences result from transcription initiation in one of two leader exons. While not altering the mature IGF-I coding sequence, these different leaders potentially encode two distinct IGF-I prepeptides, one of 48 amino acids (exon 1) and one of 32 amino acids (exon 2). Within exon 1, transcription initiation is dispersed (i.e. occurs over a approximately 350-basepair region), while within exon 2, it is highly localized. A fourth exon 1 start site, residing only approximately 30 basepairs from its 3' end, is suggested on the basis of RNase protection assays; its use would produce an mRNA encoding a third distinct IGF-I leader peptide of 22 amino acids. We have determined that during postnatal development, and as a result of insulinopenic diabetes and fasting, choice of transcription start sites within exon 1 in the liver is coordinately regulated, i.e. use of all start sites increased during development and decreased in the two catabolic states. Transcription initiation at the single major site within exon 2 was also reduced in diabetes and fasting. Insulin replacement therapy and refeeding restored the levels of all transcripts coordinately. During postnatal development, however, transcripts initiating within exon 2 exhibited a different developmental profile than did exon 1 transcripts, increasing especially at the onset of GH-dependent linear growth. In liver, therefore, negative regulation of exon 1 and exon 2 transcription start site usage occurs in catabolic states, while in development, differential regulation of exon 1 and exon 2 transcription start sites occurs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0888-8809
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1677-86
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1779970-Aging, pubmed-meshheading:1779970-Animals, pubmed-meshheading:1779970-Antisense Elements (Genetics), pubmed-meshheading:1779970-Base Sequence, pubmed-meshheading:1779970-Chromosome Deletion, pubmed-meshheading:1779970-Cloning, Molecular, pubmed-meshheading:1779970-Diabetes Mellitus, Experimental, pubmed-meshheading:1779970-Exons, pubmed-meshheading:1779970-Fasting, pubmed-meshheading:1779970-Fetus, pubmed-meshheading:1779970-Gene Expression Regulation, pubmed-meshheading:1779970-Gene Library, pubmed-meshheading:1779970-Insulin-Like Growth Factor I, pubmed-meshheading:1779970-Liver, pubmed-meshheading:1779970-Male, pubmed-meshheading:1779970-Molecular Sequence Data, pubmed-meshheading:1779970-Oligodeoxyribonucleotides, pubmed-meshheading:1779970-Protein Sorting Signals, pubmed-meshheading:1779970-RNA, Messenger, pubmed-meshheading:1779970-RNA Probes, pubmed-meshheading:1779970-RNA Processing, Post-Transcriptional, pubmed-meshheading:1779970-Rats, pubmed-meshheading:1779970-Rats, Inbred Strains, pubmed-meshheading:1779970-Restriction Mapping, pubmed-meshheading:1779970-Transcription, Genetic
pubmed:year
1991
pubmed:articleTitle
Regulation of start site usage in the leader exons of the rat insulin-like growth factor-I gene by development, fasting, and diabetes.
pubmed:affiliation
Section on Molecular and Cellular Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't