Linked Life Data

12974633

Source:http://linkedlifedata.com/resource/pubmed/id/12974633

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
37
pubmed:dateCreated
2003-9-16
pubmed:abstractText
We have quantified the basal and glucocorticoid-regulated levels of different transcripts from the human glucocorticoid receptor (GR) gene in the T-cell acute lymphoblastic leukemia cell line, CEM-C7, and in the B lymphoblastoid cell line, IM-9. Highly specific quantitative, reverse transcription-polymerase chain reaction assays measured total GR transcripts, transcripts encoding the isoforms glucocorticoid receptor alpha (GRalpha) and glucocorticoid receptor beta (GRbeta), and transcripts containing different forms of exon 1: 1A1, 1A2, 1A3, 1B, and 1C. GRalpha and GRbeta transcripts are coordinately upregulated in CEM-C7 cells and coordinately downregulated in IM-9 cells by dexamethasone. The concentration of GRalpha mRNA is more than a 1000-fold higher than that for GRbeta mRNA. Transcripts with different exon 1 forms are all upregulated in CEM-C7 cells and all downregulated in IM-9 cells by dexamethasone, but transcripts containing exons 1A1, 1A2, or 1A3 are regulated to a higher degree than transcripts containing exon 1B or exon 1C. However, exon 1B- and exon 1C-containing transcripts are substantially more abundant than exon 1A-containing transcripts, with exon 1A3-containing transcripts more abundant than exon 1A1- or exon 1A2-containing transcripts. Analysis using models for glucocorticoid receptor autoregulation kinetics suggests that the minor 1A3-containing transcript component could be important for GR protein upregulation, and hence apoptosis, in CEM-C7 cells. These studies suggest that GRalpha transcripts containing exons 1A3, 1B, and 1C contribute most to the intracellular level of GR mRNA and may be the most relevant for steroid-mediated apoptosis in T-lymphoblasts.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-2960
pubmed:author
pubmed:issnType
Print
pubmed:day
23
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10978-90
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12974633-Blotting, Western, pubmed-meshheading:12974633-DNA, Complementary, pubmed-meshheading:12974633-Dexamethasone, pubmed-meshheading:12974633-Down-Regulation, pubmed-meshheading:12974633-Exons, pubmed-meshheading:12974633-Glucocorticoids, pubmed-meshheading:12974633-Humans, pubmed-meshheading:12974633-Kinetics, pubmed-meshheading:12974633-Leukemia, pubmed-meshheading:12974633-Models, Chemical, pubmed-meshheading:12974633-Models, Genetic, pubmed-meshheading:12974633-Protein Isoforms, pubmed-meshheading:12974633-RNA, pubmed-meshheading:12974633-RNA, Messenger, pubmed-meshheading:12974633-Receptors, Glucocorticoid, pubmed-meshheading:12974633-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:12974633-T-Lymphocytes, pubmed-meshheading:12974633-Time Factors, pubmed-meshheading:12974633-Tumor Cells, Cultured, pubmed-meshheading:12974633-Up-Regulation
pubmed:year
2003
pubmed:articleTitle
Quantification and glucocorticoid regulation of glucocorticoid receptor transcripts in two human leukemic cell lines.
pubmed:affiliation
Department of Biochemistry and Molecular Biology and Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, 533 Bolivar Street, New Orleans, Louisiana 70112, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't