EGR-1, a UV-Inducible Gene in p53−/− Mouse Cells
Identifieur interne : 002647 ( Istex/Corpus ); 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
Links to Exploration step
ISTEX:A6C1C746117C06E8AB4B4FAE25EAD94B17F9A9E6Le document en format XML
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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. 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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. 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science</json:string><json:string>2 - oncology</json:string><json:string>2 - cell biology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - biochemistry & molecular biology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cell Biology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1006/excr.2001.5196</json:string></doi><id>A6C1C746117C06E8AB4B4FAE25EAD94B17F9A9E6</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-T6NPRFL1-T/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-T6NPRFL1-T/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-T6NPRFL1-T/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">EGR-1, a UV-Inducible Gene in p53−/− Mouse Cells</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©2001 Academic Press</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>2001</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Regular Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">EGR-1, a UV-Inducible Gene in p53−/− Mouse Cells</title><author xml:id="author-0000"><persName><forename type="first">Weihua</forename><surname>Zhang</surname></persName><affiliation>Laboratory for Cancer Research, College of Pharmacy, Rutgers, the State University of New Jersey, 164 Frelinghuysen Road, Piscataway, New Jersey, 08854</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Suzie</forename><surname>Chen</surname></persName><affiliation>Laboratory for Cancer Research, College of Pharmacy, Rutgers, the State University of New Jersey, 164 Frelinghuysen Road, Piscataway, New Jersey, 08854</affiliation></author><idno type="istex">A6C1C746117C06E8AB4B4FAE25EAD94B17F9A9E6</idno><idno type="ark">ark:/67375/6H6-T6NPRFL1-T</idno><idno type="DOI">10.1006/excr.2001.5196</idno><idno type="PII">S0014-4827(01)95196-1</idno></analytic><monogr><title level="j">Experimental Cell Research</title><title level="j" type="abbrev">YEXCR</title><idno type="pISSN">0014-4827</idno><idno type="PII">S0014-4827(00)X0021-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">266</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="21">21</biblScope><biblScope unit="page" to="30">30</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>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.</p></abstract></profileDesc><revisionDesc><change when="2001-01-18">Modified</change><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-T6NPRFL1-T/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>YEXCR</jid><aid>95196</aid><ce:pii>S0014-4827(01)95196-1</ce:pii><ce:doi>10.1006/excr.2001.5196</ce:doi><ce:copyright type="full-transfer" year="2001">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>EGR-1, a UV-Inducible Gene in p53<ce:sup>−/−</ce:sup> Mouse Cells</ce:title><ce:author-group><ce:author><ce:given-name>Weihua</ce:given-name><ce:surname>Zhang</ce:surname></ce:author><ce:author><ce:given-name>Suzie</ce:given-name><ce:surname>Chen</ce:surname><ce:cross-ref refid="FN1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Laboratory for Cancer Research, College of Pharmacy, Rutgers, the State University of New Jersey, 164 Frelinghuysen Road, Piscataway, New Jersey, 08854</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>To whom correspondence and reprint requests should be addressed. Fax: (732) 445-0687. E-mail: suziec@rci.rutgers.edu.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="3" month="10" year="2000"></ce:date-received><ce:date-revised day="18" month="1" year="2001"></ce:date-revised><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Changes in gene expression were examined in p53<ce:sup>−/−</ce:sup> and p53<ce:sup>+/+</ce:sup> mouse cells after ultraviolet (UV) irradiation. Differential display was used to identify differentially expressed gene(s) in UV-treated p53<ce:sup>−/−</ce:sup> and p53<ce:sup>+/+</ce:sup> cells. One of the differentially expressed genes was EGR-1 (early growth response gene-1), which was shown to be induced only in p53<ce:sup>−/−</ce:sup> 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. <ce:italic>De novo</ce:italic> protein synthesis was not required for UV-induced EGR-1 expression in p53<ce:sup>−/−</ce:sup> cells. Pretreatment of p53<ce:sup>−/−</ce:sup> 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<ce:sup>+/+</ce:sup> cells, but not in p53<ce:sup>−/−</ce:sup> 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.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>EGR-1, a UV-Inducible Gene in p53−/− Mouse Cells</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>EGR-1, a UV-Inducible Gene in p53</title></titleInfo><name type="personal"><namePart type="given">Weihua</namePart><namePart type="family">Zhang</namePart><affiliation>Laboratory for Cancer Research, College of Pharmacy, Rutgers, the State University of New Jersey, 164 Frelinghuysen Road, Piscataway, New Jersey, 08854</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Suzie</namePart><namePart type="family">Chen</namePart><affiliation>Laboratory for Cancer Research, College of Pharmacy, Rutgers, the State University of New Jersey, 164 Frelinghuysen Road, Piscataway, New Jersey, 08854</affiliation><description>To whom correspondence and reprint requests should be addressed. Fax: (732) 445-0687. E-mail: suziec@rci.rutgers.edu.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><dateModified encoding="w3cdtf">2001-01-18</dateModified><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract 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.</abstract><note type="content">Section title: Regular Article</note><relatedItem type="host"><titleInfo><title>Experimental Cell Research</title></titleInfo><titleInfo type="abbreviated"><title>YEXCR</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued></originInfo><identifier type="ISSN">0014-4827</identifier><identifier type="PII">S0014-4827(00)X0021-3</identifier><part><date>2001</date><detail type="volume"><number>266</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>201</end></extent><extent unit="pages"><start>21</start><end>30</end></extent></part></relatedItem><identifier type="istex">A6C1C746117C06E8AB4B4FAE25EAD94B17F9A9E6</identifier><identifier type="ark">ark:/67375/6H6-T6NPRFL1-T</identifier><identifier type="DOI">10.1006/excr.2001.5196</identifier><identifier type="PII">S0014-4827(01)95196-1</identifier><accessCondition type="use and reproduction" contentType="copyright">©2001 Academic Press</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, ©2001</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-T6NPRFL1-T/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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