EGR-1, a UV-Inducible Gene in p53−/− Mouse Cells
Identifieur interne : 002647 ( Istex/Curation ); précédent : 002646; suivant : 002648EGR-1, a UV-Inducible Gene in p53−/− Mouse Cells
Auteurs : Weihua Zhang ; Suzie ChenSource :
- Experimental Cell Research [ 0014-4827 ] ; 2001.
English descriptors
- Teeft :
- Acad, Apoptosis, Apoptotic, Apoptotic cell, Apoptotic cells, Assay, Blot, Boehringer mannheim, Cdna, Cdna fragments, Cell, Cell cycle arrest, Cell proliferation, Cell surface growth factor receptors, Clone, Clones transfected, Consecutive days, Constitutive expression, Control cells, Culture medium, Current study, Dark arrows, Dense foci, Differential display, Differential displays, Differential expression, Differentially, Early growth response, Exclusion assays, Fresh growth medium, Gene, Gene dosage, Gene expression, Gene status, Genotoxic stress, Growth assays, Growth factor receptors, Growth factor responses, Growth factors, Growth rate, Higher levels, Important player, Increase initiation, Induction, Inhibitory effect, Life technologies, Light arrow, Malignant progression, Mammalian cells, Mouse cells, Mouse expression, Natl, Nonapoptotic cells, Northern blot, Northern blots, Null cells, Overexpression, Pathway, Plasmid, Positive clones, Present report, Present study, Proc, Promoter, Promoter activity, Promoter region, Protein synthesis, Receptor, Same amount, Same blot reprobed, Same promoter region, Separate experiments, Serum induction, Serum response elements, Serum stimulation, Signal transduction pathways, Single copy, Skin tumors, Soft agar, Stable expression, Stress signals, Suramin, Survival rate, Time course, Total cells, Total energy, Total protein, Transcription factors, Transfected, Transformation assays, Transformation frequency, Tumor suppression, Tunel assays, Untreated, Untreated cells, Untreated controls, Uorescence microscope, Uvinduced transformation, Various promoters, Viable cells, Zhang.
Abstract
Abstract: Changes in gene expression were examined in p53−/− and p53+/+ mouse cells after ultraviolet (UV) irradiation. Differential display was used to identify differentially expressed gene(s) in UV-treated p53−/− and p53+/+ cells. One of the differentially expressed genes was EGR-1 (early growth response gene-1), which was shown to be induced only in p53−/− cells. The induction of this gene by UV was detected as early as 0.5 h, peaked at 2 h, and returned to normal levels by 4 h. De novo protein synthesis was not required for UV-induced EGR-1 expression in p53−/− cells. Pretreatment of p53−/− cells with suramin, an inhibitor of growth factor receptors, completely suppressed UV-induced EGR-1 expression, suggesting that the induction may be mediated via the growth factor receptors. The presence of wild-type p53 suppressed the induction of EGR-1 after UV treatment. Overexpression of EGR-1 promoted the UV-induced transformation in p53+/+ cells, but not in p53−/− cells. These data suggested that EGR-1 may be an important player in the UV responses of mammalian cells and may influence UV-induced transformation.
Url:
DOI: 10.1006/excr.2001.5196
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Weihua Zhang<affiliation><mods:affiliation>Laboratory for Cancer Research, College of Pharmacy, Rutgers, the State University of New Jersey, 164 Frelinghuysen Road, Piscataway, New Jersey, 08854</mods:affiliation>
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Le document en format XML
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<term>Constitutive expression</term>
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<term>Culture medium</term>
<term>Current study</term>
<term>Dark arrows</term>
<term>Dense foci</term>
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<term>Exclusion assays</term>
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<term>Proc</term>
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<term>Soft agar</term>
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<term>Suramin</term>
<term>Survival rate</term>
<term>Time course</term>
<term>Total cells</term>
<term>Total energy</term>
<term>Total protein</term>
<term>Transcription factors</term>
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<term>Transformation assays</term>
<term>Transformation frequency</term>
<term>Tumor suppression</term>
<term>Tunel assays</term>
<term>Untreated</term>
<term>Untreated cells</term>
<term>Untreated controls</term>
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<front><div type="abstract" xml:lang="en">Abstract: Changes in gene expression were examined in p53−/− and p53+/+ mouse cells after ultraviolet (UV) irradiation. Differential display was used to identify differentially expressed gene(s) in UV-treated p53−/− and p53+/+ cells. One of the differentially expressed genes was EGR-1 (early growth response gene-1), which was shown to be induced only in p53−/− cells. The induction of this gene by UV was detected as early as 0.5 h, peaked at 2 h, and returned to normal levels by 4 h. De novo protein synthesis was not required for UV-induced EGR-1 expression in p53−/− cells. Pretreatment of p53−/− cells with suramin, an inhibitor of growth factor receptors, completely suppressed UV-induced EGR-1 expression, suggesting that the induction may be mediated via the growth factor receptors. The presence of wild-type p53 suppressed the induction of EGR-1 after UV treatment. Overexpression of EGR-1 promoted the UV-induced transformation in p53+/+ cells, but not in p53−/− cells. These data suggested that EGR-1 may be an important player in the UV responses of mammalian cells and may influence UV-induced transformation.</div>
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