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A polymorphism (G-->A transition) in the -78 position of the apolipoprotein A-I promoter increases transcription efficiency
AG-->A transition at -78 base pairs from the transcription start site of the apolipoprotein A-I (apoA-I) gene has been associated with increased apoA-I serum levels in humans. We report here that this mutation (G-->A) increases significantly (5-7-fold) the expression of a reporter gene fused t...
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Published in: | The Journal of biological chemistry 1994-07, Vol.269 (26), p.17371-17374 |
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container_end_page | 17374 |
container_issue | 26 |
container_start_page | 17371 |
container_title | The Journal of biological chemistry |
container_volume | 269 |
creator | ANGOTTI, E MELE, E COSTANZO, F AVVEDIMENTO, V |
description | AG-->A transition at -78 base pairs from the transcription start site of the apolipoprotein A-I (apoA-I) gene has been associated
with increased apoA-I serum levels in humans. We report here that this mutation (G-->A) increases significantly (5-7-fold)
the expression of a reporter gene fused to the apoA-I promoter in human liver and intestine cells. In addition, the presence
of A at -78 base pairs from the transcription start site of the gene significantly decreases the binding affinity of a nuclear
factor present in liver and intestine cells. We suggest that the reduced affinity of this factor increases the transcription
efficiency of the promoter and explains why individuals carrying the A allele have high serum apoA-I levels. |
doi_str_mv | 10.1016/s0021-9258(17)32445-6 |
format | article |
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with increased apoA-I serum levels in humans. We report here that this mutation (G-->A) increases significantly (5-7-fold)
the expression of a reporter gene fused to the apoA-I promoter in human liver and intestine cells. In addition, the presence
of A at -78 base pairs from the transcription start site of the gene significantly decreases the binding affinity of a nuclear
factor present in liver and intestine cells. We suggest that the reduced affinity of this factor increases the transcription
efficiency of the promoter and explains why individuals carrying the A allele have high serum apoA-I levels.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/s0021-9258(17)32445-6</identifier><identifier>PMID: 8021234</identifier><identifier>CODEN: JBCHA3</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Biochemistry and Molecular Biology</publisher><subject>Adenine ; Apolipoprotein A-I - genetics ; Apolipoprotein A-I - metabolism ; Base Sequence ; Biological and medical sciences ; Fundamental and applied biological sciences. Psychology ; Guanine ; Humans ; Molecular and cellular biology ; Molecular genetics ; Molecular Sequence Data ; Mutation ; Nuclear Proteins - metabolism ; Oligodeoxyribonucleotides ; Point Mutation ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Transcription, Genetic ; Transcription. Transcription factor. Splicing. Rna processing ; Tumor Cells, Cultured</subject><ispartof>The Journal of biological chemistry, 1994-07, Vol.269 (26), p.17371-17374</ispartof><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-dc8262fbf43acd328471255c82aa89d3ffdb669d75bf9354346eb89fcf73e0a33</citedby><cites>FETCH-LOGICAL-c506t-dc8262fbf43acd328471255c82aa89d3ffdb669d75bf9354346eb89fcf73e0a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4215999$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8021234$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ANGOTTI, E</creatorcontrib><creatorcontrib>MELE, E</creatorcontrib><creatorcontrib>COSTANZO, F</creatorcontrib><creatorcontrib>AVVEDIMENTO, V</creatorcontrib><title>A polymorphism (G-->A transition) in the -78 position of the apolipoprotein A-I promoter increases transcription efficiency</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>AG-->A transition at -78 base pairs from the transcription start site of the apolipoprotein A-I (apoA-I) gene has been associated
with increased apoA-I serum levels in humans. We report here that this mutation (G-->A) increases significantly (5-7-fold)
the expression of a reporter gene fused to the apoA-I promoter in human liver and intestine cells. In addition, the presence
of A at -78 base pairs from the transcription start site of the gene significantly decreases the binding affinity of a nuclear
factor present in liver and intestine cells. We suggest that the reduced affinity of this factor increases the transcription
efficiency of the promoter and explains why individuals carrying the A allele have high serum apoA-I levels.</description><subject>Adenine</subject><subject>Apolipoprotein A-I - genetics</subject><subject>Apolipoprotein A-I - metabolism</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guanine</subject><subject>Humans</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oligodeoxyribonucleotides</subject><subject>Point Mutation</subject><subject>Polymorphism, Genetic</subject><subject>Promoter Regions, Genetic</subject><subject>Transcription, Genetic</subject><subject>Transcription. Transcription factor. Splicing. Rna processing</subject><subject>Tumor Cells, Cultured</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><recordid>eNqFkctq3DAUhkVpSCZpHyHgRSjJQonusjaFITQXCHSRFroTsizFCrblSh7KkJev5sJkGYGQ9J_vP0ecA8A5RtcYYXGTESIYKsLrSyyvKGGMQ_EJLDCqKaQc__kMFgfkBJzm_IrKYgofg-O6BAhlC_C2rKbYr4eYpi7kobq8h_D7spqTGXOYQxyvqjBWc-cqKOuC7sQq-q1mijdMcUpxdgVbwseq3IfySsVmkzPZ5V0ym8K0tTrvgw1utOsv4MibPruv-_MM_L778ev2AT79vH-8XT5By5GYYWtrIohvPKPGtpTUTGLCeVGNqVVLvW8bIVQreeMV5Ywy4ZpaeesldchQega-7fKWv_1duTzrIWTr-t6MLq6yloJLJgn_EMRCUaWYKiDfgTbFnJPzekphMGmtMdKb6ejnTev1pvUaS72djhbFd74vsGoG1x5c-3GU-MU-brI1vS-NsyEfMEYwV0q9Y1146f6F5HQTou3coIlQZZeSVGL6HxZBpCo</recordid><startdate>19940701</startdate><enddate>19940701</enddate><creator>ANGOTTI, E</creator><creator>MELE, E</creator><creator>COSTANZO, F</creator><creator>AVVEDIMENTO, V</creator><general>American Society for Biochemistry and Molecular Biology</general><scope>IQODW</scope><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>7TM</scope><scope>7X8</scope></search><sort><creationdate>19940701</creationdate><title>A polymorphism (G-->A transition) in the -78 position of the apolipoprotein A-I promoter increases transcription efficiency</title><author>ANGOTTI, E ; MELE, E ; COSTANZO, F ; AVVEDIMENTO, V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-dc8262fbf43acd328471255c82aa89d3ffdb669d75bf9354346eb89fcf73e0a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Adenine</topic><topic>Apolipoprotein A-I - genetics</topic><topic>Apolipoprotein A-I - metabolism</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guanine</topic><topic>Humans</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Nuclear Proteins - metabolism</topic><topic>Oligodeoxyribonucleotides</topic><topic>Point Mutation</topic><topic>Polymorphism, Genetic</topic><topic>Promoter Regions, Genetic</topic><topic>Transcription, Genetic</topic><topic>Transcription. Transcription factor. Splicing. Rna processing</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ANGOTTI, E</creatorcontrib><creatorcontrib>MELE, E</creatorcontrib><creatorcontrib>COSTANZO, F</creatorcontrib><creatorcontrib>AVVEDIMENTO, V</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ANGOTTI, E</au><au>MELE, E</au><au>COSTANZO, F</au><au>AVVEDIMENTO, V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A polymorphism (G-->A transition) in the -78 position of the apolipoprotein A-I promoter increases transcription efficiency</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1994-07-01</date><risdate>1994</risdate><volume>269</volume><issue>26</issue><spage>17371</spage><epage>17374</epage><pages>17371-17374</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><coden>JBCHA3</coden><abstract>AG-->A transition at -78 base pairs from the transcription start site of the apolipoprotein A-I (apoA-I) gene has been associated
with increased apoA-I serum levels in humans. We report here that this mutation (G-->A) increases significantly (5-7-fold)
the expression of a reporter gene fused to the apoA-I promoter in human liver and intestine cells. In addition, the presence
of A at -78 base pairs from the transcription start site of the gene significantly decreases the binding affinity of a nuclear
factor present in liver and intestine cells. We suggest that the reduced affinity of this factor increases the transcription
efficiency of the promoter and explains why individuals carrying the A allele have high serum apoA-I levels.</abstract><cop>Bethesda, MD</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>8021234</pmid><doi>10.1016/s0021-9258(17)32445-6</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenine Apolipoprotein A-I - genetics Apolipoprotein A-I - metabolism Base Sequence Biological and medical sciences Fundamental and applied biological sciences. Psychology Guanine Humans Molecular and cellular biology Molecular genetics Molecular Sequence Data Mutation Nuclear Proteins - metabolism Oligodeoxyribonucleotides Point Mutation Polymorphism, Genetic Promoter Regions, Genetic Transcription, Genetic Transcription. Transcription factor. Splicing. Rna processing Tumor Cells, Cultured |
title | A polymorphism (G-->A transition) in the -78 position of the apolipoprotein A-I promoter increases transcription efficiency |
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