CpG methylation inhibits proenkephalin gene expression and binding of the transcription factor AP-2
DNA methylation at HpaII (CmCGG) sites inhibits expression of a human proenkephalin-CAT fusion gene when it is transiently expressed in CV-1 cells or stably expressed in C6-glioma cells. The inhibitory effects of HpaII methylation have been mapped to a site within the human proenkephalin promoter lo...
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| Veröffentlicht in: | Nucleic acids research 1990-07, Vol.18 (13), p.3975-3982 |
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| creator | COMB, M GOODMAN, H. M |
| description | DNA methylation at HpaII (CmCGG) sites inhibits expression of a human proenkephalin-CAT fusion gene when it is transiently expressed in CV-1 cells or stably expressed in C6-glioma cells. The inhibitory effects of HpaII methylation have been mapped to a site within the human proenkephalin promoter located at position -72 relative to the start site of transcription. This region spans a cAMP and phorbol ester inducible enhancer and methylation at this position inhibits both basal transcription and transcription induced by either cAMP or TPA. The HpaII site is located within an element which binds the transcription factor AP-2. In vitro methylation at this HpaII site inhibits the binding of AP-2. These results suggest that CpG methylation inhibits proenkephalin gene expression by directly interfering with the binding of a positively acting transcription factor previously shown to be essential for maximal basal, cAMP, and TPA inducible transcription. |
| doi_str_mv | 10.1093/nar/18.13.3975 |
| format | Article |
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M</creator><creatorcontrib>COMB, M ; GOODMAN, H. M</creatorcontrib><description>DNA methylation at HpaII (CmCGG) sites inhibits expression of a human proenkephalin-CAT fusion gene when it is transiently expressed in CV-1 cells or stably expressed in C6-glioma cells. The inhibitory effects of HpaII methylation have been mapped to a site within the human proenkephalin promoter located at position -72 relative to the start site of transcription. This region spans a cAMP and phorbol ester inducible enhancer and methylation at this position inhibits both basal transcription and transcription induced by either cAMP or TPA. The HpaII site is located within an element which binds the transcription factor AP-2. In vitro methylation at this HpaII site inhibits the binding of AP-2. These results suggest that CpG methylation inhibits proenkephalin gene expression by directly interfering with the binding of a positively acting transcription factor previously shown to be essential for maximal basal, cAMP, and TPA inducible transcription.</description><identifier>ISSN: 0305-1048</identifier><identifier>EISSN: 1362-4962</identifier><identifier>DOI: 10.1093/nar/18.13.3975</identifier><identifier>PMID: 1695733</identifier><identifier>CODEN: NARHAD</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>5-Methylcytosine ; Base Sequence ; Biological and medical sciences ; Cloning, Molecular ; Cytosine - analogs & derivatives ; Cytosine - metabolism ; Deoxyribonuclease HpaII ; Deoxyribonucleases, Type II Site-Specific - metabolism ; Dinucleoside Phosphates - metabolism ; DNA - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Enkephalins - genetics ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation ; Humans ; Methylation ; Molecular and cellular biology ; Molecular genetics ; Molecular Sequence Data ; Promoter Regions, Genetic ; Protein Precursors - genetics ; Restriction Mapping ; Transcription Factor AP-2 ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transcription, Genetic ; Transcription. Transcription factor. Splicing. 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M</creatorcontrib><title>CpG methylation inhibits proenkephalin gene expression and binding of the transcription factor AP-2</title><title>Nucleic acids research</title><addtitle>Nucleic Acids Res</addtitle><description>DNA methylation at HpaII (CmCGG) sites inhibits expression of a human proenkephalin-CAT fusion gene when it is transiently expressed in CV-1 cells or stably expressed in C6-glioma cells. The inhibitory effects of HpaII methylation have been mapped to a site within the human proenkephalin promoter located at position -72 relative to the start site of transcription. This region spans a cAMP and phorbol ester inducible enhancer and methylation at this position inhibits both basal transcription and transcription induced by either cAMP or TPA. The HpaII site is located within an element which binds the transcription factor AP-2. In vitro methylation at this HpaII site inhibits the binding of AP-2. These results suggest that CpG methylation inhibits proenkephalin gene expression by directly interfering with the binding of a positively acting transcription factor previously shown to be essential for maximal basal, cAMP, and TPA inducible transcription.</description><subject>5-Methylcytosine</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Cloning, Molecular</subject><subject>Cytosine - analogs & derivatives</subject><subject>Cytosine - metabolism</subject><subject>Deoxyribonuclease HpaII</subject><subject>Deoxyribonucleases, Type II Site-Specific - metabolism</subject><subject>Dinucleoside Phosphates - metabolism</subject><subject>DNA - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Enkephalins - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Methylation</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Molecular Sequence Data</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Precursors - genetics</subject><subject>Restriction Mapping</subject><subject>Transcription Factor AP-2</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic</subject><subject>Transcription. Transcription factor. Splicing. Rna processing</subject><subject>Tumor Cells, Cultured</subject><issn>0305-1048</issn><issn>1362-4962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkT1vFDEQhi1EFI5AS4fkBrq92DtefxQU0QkCUqSkgNryemdvDXvexd5D5N_j406EVKlcvM87Gs9DyBvO1pwZuIwuXXK95rAGo5pnZMVB1pUwsn5OVgxYU3Em9AvyMufvjHHBG3FOzrk0jQJYEb-Zr-kOl-F-dEuYIg1xCG1YMp3ThPEHzoMbQ6RbjEjx95ww5wPmYkfbELsQt3Tq6TIgXZKL2acw_53TO79MiV7dVfUrcta7MePr03tBvn36-HXzubq5vf6yubqpvFByqYwEZ5TWTjCpJOuM7IG5tu50b6TSHSrU3reSlaxHBActr7HmBjqNKD1ckA_HufO-3WHnMZaVRjunsHPp3k4u2MdJDIPdTr8sAOeMl_77Uz9NP_eYF7sL2eM4uojTPltltFHA2JMgL9fXtRBPg43RUFwVcH0EfZpyTtj_25oze_Bsi2fLteVgD55L4e3_f33Aj2JL_u6Uu-zd2Bc3PuQHzNRSCyngD0rIsv0</recordid><startdate>19900711</startdate><enddate>19900711</enddate><creator>COMB, M</creator><creator>GOODMAN, H. M</creator><general>Oxford University Press</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19900711</creationdate><title>CpG methylation inhibits proenkephalin gene expression and binding of the transcription factor AP-2</title><author>COMB, M ; GOODMAN, H. M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-963a9788a406760d96f30ab2d8f9678de7e8ccb6060dfee3a3b12e2193d8ee6c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>5-Methylcytosine</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Cloning, Molecular</topic><topic>Cytosine - analogs & derivatives</topic><topic>Cytosine - metabolism</topic><topic>Deoxyribonuclease HpaII</topic><topic>Deoxyribonucleases, Type II Site-Specific - metabolism</topic><topic>Dinucleoside Phosphates - metabolism</topic><topic>DNA - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Enkephalins - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Methylation</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Molecular Sequence Data</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Precursors - genetics</topic><topic>Restriction Mapping</topic><topic>Transcription Factor AP-2</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</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>COMB, M</creatorcontrib><creatorcontrib>GOODMAN, H. 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M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CpG methylation inhibits proenkephalin gene expression and binding of the transcription factor AP-2</atitle><jtitle>Nucleic acids research</jtitle><addtitle>Nucleic Acids Res</addtitle><date>1990-07-11</date><risdate>1990</risdate><volume>18</volume><issue>13</issue><spage>3975</spage><epage>3982</epage><pages>3975-3982</pages><issn>0305-1048</issn><eissn>1362-4962</eissn><coden>NARHAD</coden><abstract>DNA methylation at HpaII (CmCGG) sites inhibits expression of a human proenkephalin-CAT fusion gene when it is transiently expressed in CV-1 cells or stably expressed in C6-glioma cells. The inhibitory effects of HpaII methylation have been mapped to a site within the human proenkephalin promoter located at position -72 relative to the start site of transcription. This region spans a cAMP and phorbol ester inducible enhancer and methylation at this position inhibits both basal transcription and transcription induced by either cAMP or TPA. The HpaII site is located within an element which binds the transcription factor AP-2. In vitro methylation at this HpaII site inhibits the binding of AP-2. These results suggest that CpG methylation inhibits proenkephalin gene expression by directly interfering with the binding of a positively acting transcription factor previously shown to be essential for maximal basal, cAMP, and TPA inducible transcription.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>1695733</pmid><doi>10.1093/nar/18.13.3975</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Nucleic acids research, 1990-07, Vol.18 (13), p.3975-3982 |
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| source | MEDLINE; Oxford University Press Journals Digital Archive Legacy; PubMed Central |
| subjects | 5-Methylcytosine Base Sequence Biological and medical sciences Cloning, Molecular Cytosine - analogs & derivatives Cytosine - metabolism Deoxyribonuclease HpaII Deoxyribonucleases, Type II Site-Specific - metabolism Dinucleoside Phosphates - metabolism DNA - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Enkephalins - genetics Fundamental and applied biological sciences. Psychology Gene Expression Regulation Humans Methylation Molecular and cellular biology Molecular genetics Molecular Sequence Data Promoter Regions, Genetic Protein Precursors - genetics Restriction Mapping Transcription Factor AP-2 Transcription Factors - genetics Transcription Factors - metabolism Transcription, Genetic Transcription. Transcription factor. Splicing. Rna processing Tumor Cells, Cultured |
| title | CpG methylation inhibits proenkephalin gene expression and binding of the transcription factor AP-2 |
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