Role of Far Upstream Repressor Elements Controlling Proto-Ha-ras Gene Transcription
The far upstream region of the rat Ha-rasgene has been characterized to determine whether possible repressor sequences may control the low level of Ha-rasgene transcription from its TATA-less, GC-rich strong promoter. The chloramphenicol acetyl transferase (CAT) gene under the control of the 3.8-kb...
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| Veröffentlicht in: | Biochemical and biophysical research communications 1998-11, Vol.252 (3), p.716-722 |
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| creator | Chakraborty, Asit K. Hodgson, Clague P. |
| description | The far upstream region of the rat Ha-rasgene has been characterized to determine whether possible repressor sequences may control the low level of Ha-rasgene transcription from its TATA-less, GC-rich strong promoter. The chloramphenicol acetyl transferase (CAT) gene under the control of the 3.8-kb Ha-rasupstream promoter was minimally expressed in HeLa cells. Surprisingly, CAT gene expression was increased by the deletion of a 0.7-kbBglII fragment containing non-coding exon minus 2 and TATA box promoter elements located 1.7 kb upstream of the GC-rich strong promoter. Far upstream (CA)25repeats also appeared to repress Ha-rasgene activity. Sequences within the 0.7-kbBglII fragment suppressed CAT gene expression when placed upstream of a heterologous thymidine kinase (tk) gene promoter. Repressor activity was further localized to a 160-bpAvrII-BglII sub-fragment. Gel shift assays identified two sequence-specific DNA binding proteins. The results demonstrated for the first time that far upstream repressor sequences control normal transcription of the Ha-rasproto-oncogene. |
| doi_str_mv | 10.1006/bbrc.1998.9711 |
| format | Article |
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The chloramphenicol acetyl transferase (CAT) gene under the control of the 3.8-kb Ha-rasupstream promoter was minimally expressed in HeLa cells. Surprisingly, CAT gene expression was increased by the deletion of a 0.7-kbBglII fragment containing non-coding exon minus 2 and TATA box promoter elements located 1.7 kb upstream of the GC-rich strong promoter. Far upstream (CA)25repeats also appeared to repress Ha-rasgene activity. Sequences within the 0.7-kbBglII fragment suppressed CAT gene expression when placed upstream of a heterologous thymidine kinase (tk) gene promoter. Repressor activity was further localized to a 160-bpAvrII-BglII sub-fragment. Gel shift assays identified two sequence-specific DNA binding proteins. The results demonstrated for the first time that far upstream repressor sequences control normal transcription of the Ha-rasproto-oncogene.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.1998.9711</identifier><identifier>PMID: 9837772</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Bacterial Proteins ; Chloramphenicol O-Acetyltransferase - genetics ; Deoxyribonuclease BamHI - metabolism ; Deoxyribonuclease HindIII - metabolism ; Deoxyribonucleases, Type II Site-Specific - metabolism ; Gene Expression Regulation ; Genes, ras - genetics ; Ha-ras ; oncogene ; Promoter Regions, Genetic ; Rats ; Repressor Proteins - physiology ; Sequence Analysis, DNA ; Transcription, Genetic ; transcriptional regulation</subject><ispartof>Biochemical and biophysical research communications, 1998-11, Vol.252 (3), p.716-722</ispartof><rights>1998 Academic Press</rights><rights>Copyright 1998 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c339t-41d39a633450a3fb0b292054964a3951a2511d207710b594a48c7fdb9f6919f63</citedby><cites>FETCH-LOGICAL-c339t-41d39a633450a3fb0b292054964a3951a2511d207710b594a48c7fdb9f6919f63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/bbrc.1998.9711$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9837772$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chakraborty, Asit K.</creatorcontrib><creatorcontrib>Hodgson, Clague P.</creatorcontrib><title>Role of Far Upstream Repressor Elements Controlling Proto-Ha-ras Gene Transcription</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The far upstream region of the rat Ha-rasgene has been characterized to determine whether possible repressor sequences may control the low level of Ha-rasgene transcription from its TATA-less, GC-rich strong promoter. The chloramphenicol acetyl transferase (CAT) gene under the control of the 3.8-kb Ha-rasupstream promoter was minimally expressed in HeLa cells. Surprisingly, CAT gene expression was increased by the deletion of a 0.7-kbBglII fragment containing non-coding exon minus 2 and TATA box promoter elements located 1.7 kb upstream of the GC-rich strong promoter. Far upstream (CA)25repeats also appeared to repress Ha-rasgene activity. Sequences within the 0.7-kbBglII fragment suppressed CAT gene expression when placed upstream of a heterologous thymidine kinase (tk) gene promoter. Repressor activity was further localized to a 160-bpAvrII-BglII sub-fragment. Gel shift assays identified two sequence-specific DNA binding proteins. The results demonstrated for the first time that far upstream repressor sequences control normal transcription of the Ha-rasproto-oncogene.</description><subject>Animals</subject><subject>Bacterial Proteins</subject><subject>Chloramphenicol O-Acetyltransferase - genetics</subject><subject>Deoxyribonuclease BamHI - metabolism</subject><subject>Deoxyribonuclease HindIII - metabolism</subject><subject>Deoxyribonucleases, Type II Site-Specific - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Genes, ras - genetics</subject><subject>Ha-ras</subject><subject>oncogene</subject><subject>Promoter Regions, Genetic</subject><subject>Rats</subject><subject>Repressor Proteins - physiology</subject><subject>Sequence Analysis, DNA</subject><subject>Transcription, Genetic</subject><subject>transcriptional regulation</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1r3EAMhofSkmw-rr0F5tSbN5LHH6tjWfIFgZQ0gd6G8VguU2yPq_EG8u_rZZfecpEO76MX9Cj1FWGNANV104hfI9FmTTXiJ7VCIMhyhOKzWsFCZDnhr1N1ltIfAMSiohN1QhtT13W-Uj-fY886dvrWiX6d0izsBv3Mk3BKUfRNzwOPc9LbOM4S-z6Mv_UPiXPM7l0mLuk7Hlm_iBuTlzDNIY4X6kvn-sSXx32uXm9vXrb32ePT3cP2-2PmjaE5K7A15CpjihKc6RpocsqhLKgqnKESXV4itjnUNUJTUuGKja-7tqGuIlyGOVffDr2TxL87TrMdQvLc927kuEu2BiCqqFzA9QH0ElMS7uwkYXDybhHs3qLdW7R7i3ZvcTm4OjbvmoHb__hR25JvDjkv770FFpt84NFzG4T9bNsYPqr-B1Rjf_E</recordid><startdate>19981127</startdate><enddate>19981127</enddate><creator>Chakraborty, Asit K.</creator><creator>Hodgson, Clague P.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19981127</creationdate><title>Role of Far Upstream Repressor Elements Controlling Proto-Ha-ras Gene Transcription</title><author>Chakraborty, Asit K. ; Hodgson, Clague P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c339t-41d39a633450a3fb0b292054964a3951a2511d207710b594a48c7fdb9f6919f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Bacterial Proteins</topic><topic>Chloramphenicol O-Acetyltransferase - genetics</topic><topic>Deoxyribonuclease BamHI - metabolism</topic><topic>Deoxyribonuclease HindIII - metabolism</topic><topic>Deoxyribonucleases, Type II Site-Specific - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Genes, ras - genetics</topic><topic>Ha-ras</topic><topic>oncogene</topic><topic>Promoter Regions, Genetic</topic><topic>Rats</topic><topic>Repressor Proteins - physiology</topic><topic>Sequence Analysis, DNA</topic><topic>Transcription, Genetic</topic><topic>transcriptional regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chakraborty, Asit K.</creatorcontrib><creatorcontrib>Hodgson, Clague P.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chakraborty, Asit K.</au><au>Hodgson, Clague P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Far Upstream Repressor Elements Controlling Proto-Ha-ras Gene Transcription</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>1998-11-27</date><risdate>1998</risdate><volume>252</volume><issue>3</issue><spage>716</spage><epage>722</epage><pages>716-722</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The far upstream region of the rat Ha-rasgene has been characterized to determine whether possible repressor sequences may control the low level of Ha-rasgene transcription from its TATA-less, GC-rich strong promoter. The chloramphenicol acetyl transferase (CAT) gene under the control of the 3.8-kb Ha-rasupstream promoter was minimally expressed in HeLa cells. Surprisingly, CAT gene expression was increased by the deletion of a 0.7-kbBglII fragment containing non-coding exon minus 2 and TATA box promoter elements located 1.7 kb upstream of the GC-rich strong promoter. Far upstream (CA)25repeats also appeared to repress Ha-rasgene activity. Sequences within the 0.7-kbBglII fragment suppressed CAT gene expression when placed upstream of a heterologous thymidine kinase (tk) gene promoter. Repressor activity was further localized to a 160-bpAvrII-BglII sub-fragment. Gel shift assays identified two sequence-specific DNA binding proteins. The results demonstrated for the first time that far upstream repressor sequences control normal transcription of the Ha-rasproto-oncogene.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>9837772</pmid><doi>10.1006/bbrc.1998.9711</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Bacterial Proteins Chloramphenicol O-Acetyltransferase - genetics Deoxyribonuclease BamHI - metabolism Deoxyribonuclease HindIII - metabolism Deoxyribonucleases, Type II Site-Specific - metabolism Gene Expression Regulation Genes, ras - genetics Ha-ras oncogene Promoter Regions, Genetic Rats Repressor Proteins - physiology Sequence Analysis, DNA Transcription, Genetic transcriptional regulation |
| title | Role of Far Upstream Repressor Elements Controlling Proto-Ha-ras Gene Transcription |
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