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- W2023991614 abstract "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 α (GRα) and glucocorticoid receptor β (GRβ), and transcripts containing different forms of exon 1: 1A1, 1A2, 1A3, 1B, and 1C. GRα and GRβ transcripts are coordinately upregulated in CEM-C7 cells and coordinately downregulated in IM-9 cells by dexamethasone. The concentration of GRα mRNA is more than a 1000-fold higher than that for GRβ 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 GRα 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." @default.
- W2023991614 created "2016-06-24" @default.
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- W2023991614 date "2003-08-21" @default.
- W2023991614 modified "2023-09-26" @default.
- W2023991614 title "Quantification and Glucocorticoid Regulation of Glucocorticoid Receptor Transcripts in Two Human Leukemic Cell Lines" @default.
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- W2023991614 doi "https://doi.org/10.1021/bi034651u" @default.
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