E-proteins directly regulate expression of activation-induced deaminase in mature B cells
Activated mature B cells in which the DNA-binding activity of E-proteins has been disrupted fail to undergo class switch recombination. Here we show that activated B cells overexpressing the antagonist helix-loop-helix protein Id3 do not induce expression of the murine Aicda gene encoding activation...
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| Veröffentlicht in: | Nature immunology 2003-06, Vol.4 (6), p.586-593 |
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| creator | Murre, Cornelis Sayegh, Camil Elie Quong, Melanie W Agata, Yasutoshi |
| description | Activated mature B cells in which the DNA-binding activity of E-proteins has been disrupted fail to undergo class switch recombination. Here we show that activated B cells overexpressing the antagonist helix-loop-helix protein Id3 do not induce expression of the murine
Aicda
gene encoding activation-induced deaminase (AID). A highly conserved intronic regulatory element in
Aicda
binds E-proteins both
in vitro
and
in vivo
. The transcriptional activity of this element is regulated by E-proteins. We show that the enforced expression of AID in cells overexpressing Id3 partially restores class switch recombination. Taken together, our observations link helix-loop-helix activity and
Aicda
gene expression in a common pathway, in which E-protein activity is required for the efficient induction of
Aicda
transcription. |
| doi_str_mv | 10.1038/ni923 |
| format | Article |
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Aicda
gene encoding activation-induced deaminase (AID). A highly conserved intronic regulatory element in
Aicda
binds E-proteins both
in vitro
and
in vivo
. The transcriptional activity of this element is regulated by E-proteins. We show that the enforced expression of AID in cells overexpressing Id3 partially restores class switch recombination. Taken together, our observations link helix-loop-helix activity and
Aicda
gene expression in a common pathway, in which E-protein activity is required for the efficient induction of
Aicda
transcription.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/ni923</identifier><identifier>PMID: 12717431</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Animals ; B-Lymphocytes - immunology ; B-Lymphocytes - metabolism ; Base Sequence ; Biomedical and Life Sciences ; Biomedicine ; Cytidine Deaminase - biosynthesis ; Cytidine Deaminase - genetics ; Cytidine Deaminase - metabolism ; Deoxyribonucleic acid ; DNA ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - immunology ; Enhancer Elements, Genetic - immunology ; Enzyme Activation ; Female ; Gene Expression Regulation, Enzymologic - immunology ; Helix-Loop-Helix Motifs - immunology ; Immunoglobulin Class Switching - immunology ; Immunoglobulin Isotypes - immunology ; Immunology ; Infectious Diseases ; Lymphocyte Activation - immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Proteins ; Signal Transduction - immunology ; TCF Transcription Factors ; Transcription Factor 7-Like 1 Protein ; Transcription Factors - genetics ; Transcription Factors - immunology</subject><ispartof>Nature immunology, 2003-06, Vol.4 (6), p.586-593</ispartof><rights>Springer Nature America, Inc. 2003</rights><rights>COPYRIGHT 2003 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-e096ed3409b823af3123747cbf54048d0bbefd161b6d9c743b1ae7c105f9f7243</citedby><cites>FETCH-LOGICAL-c455t-e096ed3409b823af3123747cbf54048d0bbefd161b6d9c743b1ae7c105f9f7243</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2727,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12717431$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Murre, Cornelis</creatorcontrib><creatorcontrib>Sayegh, Camil Elie</creatorcontrib><creatorcontrib>Quong, Melanie W</creatorcontrib><creatorcontrib>Agata, Yasutoshi</creatorcontrib><title>E-proteins directly regulate expression of activation-induced deaminase in mature B cells</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><addtitle>Nat Immunol</addtitle><description>Activated mature B cells in which the DNA-binding activity of E-proteins has been disrupted fail to undergo class switch recombination. Here we show that activated B cells overexpressing the antagonist helix-loop-helix protein Id3 do not induce expression of the murine
Aicda
gene encoding activation-induced deaminase (AID). A highly conserved intronic regulatory element in
Aicda
binds E-proteins both
in vitro
and
in vivo
. The transcriptional activity of this element is regulated by E-proteins. We show that the enforced expression of AID in cells overexpressing Id3 partially restores class switch recombination. Taken together, our observations link helix-loop-helix activity and
Aicda
gene expression in a common pathway, in which E-protein activity is required for the efficient induction of
Aicda
transcription.</description><subject>Animals</subject><subject>B-Lymphocytes - immunology</subject><subject>B-Lymphocytes - metabolism</subject><subject>Base Sequence</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cytidine Deaminase - biosynthesis</subject><subject>Cytidine Deaminase - genetics</subject><subject>Cytidine Deaminase - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - immunology</subject><subject>Enhancer Elements, Genetic - immunology</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>Gene Expression Regulation, Enzymologic - immunology</subject><subject>Helix-Loop-Helix Motifs - immunology</subject><subject>Immunoglobulin Class Switching - immunology</subject><subject>Immunoglobulin Isotypes - immunology</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><subject>Lymphocyte Activation - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular Sequence Data</subject><subject>Proteins</subject><subject>Signal Transduction - immunology</subject><subject>TCF Transcription Factors</subject><subject>Transcription Factor 7-Like 1 Protein</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - immunology</subject><issn>1529-2908</issn><issn>1529-2916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkUtr3TAQhUVpaB7NLygUUWigC6d62bKXaUiaQKDQx6IrIUuji4It30pySP59dONLLsmmaCGN5pvDHA5Cx5ScUsLbr8F3jL9BB7RmXcU62rx9fpN2Hx2mdEsIFbIR79A-ZZJKwekB-ntRreOUwYeErY9g8vCAI6zmQWfAcL-OkJKfAp4c1ib7O51LVflgZwMWW9CjDzoB9gGPOs8R8DdsYBjSe7Tn9JDgeHsfoT-XF7_Pr6qbH9-vz89uKiPqOldAugYsF6TrW8a145RxKaTpXS2IaC3pe3CWNrRvbGfK0j3VIA0lteucZIIfoZNFt_j4N0PKavRps4EOMM1JSc5ZUZb_BWnbkrphdQE_vQJvpzmGYkIxxmRNO7FRO12glR5A-eCmHLUpx8LozRTA-fJ_VkRb0oqalYEvLwYKk-E-r_Sckrr-9fMl-3lhTZxSiuDUOvpRxwdFidrErZ7iLtzH7aZzP4LdUdt8d55TaYUVxJ2V10ofFjA8hfistHQfAeEfuZE</recordid><startdate>20030601</startdate><enddate>20030601</enddate><creator>Murre, Cornelis</creator><creator>Sayegh, Camil Elie</creator><creator>Quong, Melanie W</creator><creator>Agata, Yasutoshi</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030601</creationdate><title>E-proteins directly regulate expression of activation-induced deaminase in mature B cells</title><author>Murre, Cornelis ; Sayegh, Camil Elie ; Quong, Melanie W ; Agata, Yasutoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-e096ed3409b823af3123747cbf54048d0bbefd161b6d9c743b1ae7c105f9f7243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>B-Lymphocytes - immunology</topic><topic>B-Lymphocytes - metabolism</topic><topic>Base Sequence</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cytidine Deaminase - biosynthesis</topic><topic>Cytidine Deaminase - genetics</topic><topic>Cytidine Deaminase - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - immunology</topic><topic>Enhancer Elements, Genetic - immunology</topic><topic>Enzyme Activation</topic><topic>Female</topic><topic>Gene Expression Regulation, Enzymologic - immunology</topic><topic>Helix-Loop-Helix Motifs - immunology</topic><topic>Immunoglobulin Class Switching - immunology</topic><topic>Immunoglobulin Isotypes - immunology</topic><topic>Immunology</topic><topic>Infectious Diseases</topic><topic>Lymphocyte Activation - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular Sequence Data</topic><topic>Proteins</topic><topic>Signal Transduction - 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Academic</collection><jtitle>Nature immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Murre, Cornelis</au><au>Sayegh, Camil Elie</au><au>Quong, Melanie W</au><au>Agata, Yasutoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>E-proteins directly regulate expression of activation-induced deaminase in mature B cells</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><addtitle>Nat Immunol</addtitle><date>2003-06-01</date><risdate>2003</risdate><volume>4</volume><issue>6</issue><spage>586</spage><epage>593</epage><pages>586-593</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>Activated mature B cells in which the DNA-binding activity of E-proteins has been disrupted fail to undergo class switch recombination. Here we show that activated B cells overexpressing the antagonist helix-loop-helix protein Id3 do not induce expression of the murine
Aicda
gene encoding activation-induced deaminase (AID). A highly conserved intronic regulatory element in
Aicda
binds E-proteins both
in vitro
and
in vivo
. The transcriptional activity of this element is regulated by E-proteins. We show that the enforced expression of AID in cells overexpressing Id3 partially restores class switch recombination. Taken together, our observations link helix-loop-helix activity and
Aicda
gene expression in a common pathway, in which E-protein activity is required for the efficient induction of
Aicda
transcription.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>12717431</pmid><doi>10.1038/ni923</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1529-2908 |
| ispartof | Nature immunology, 2003-06, Vol.4 (6), p.586-593 |
| issn | 1529-2908 1529-2916 |
| language | eng |
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| source | MEDLINE; Nature; Alma/SFX Local Collection |
| subjects | Animals B-Lymphocytes - immunology B-Lymphocytes - metabolism Base Sequence Biomedical and Life Sciences Biomedicine Cytidine Deaminase - biosynthesis Cytidine Deaminase - genetics Cytidine Deaminase - metabolism Deoxyribonucleic acid DNA DNA-Binding Proteins - genetics DNA-Binding Proteins - immunology Enhancer Elements, Genetic - immunology Enzyme Activation Female Gene Expression Regulation, Enzymologic - immunology Helix-Loop-Helix Motifs - immunology Immunoglobulin Class Switching - immunology Immunoglobulin Isotypes - immunology Immunology Infectious Diseases Lymphocyte Activation - immunology Mice Mice, Inbred C57BL Molecular Sequence Data Proteins Signal Transduction - immunology TCF Transcription Factors Transcription Factor 7-Like 1 Protein Transcription Factors - genetics Transcription Factors - immunology |
| title | E-proteins directly regulate expression of activation-induced deaminase in mature B cells |
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