Sp and GATA factors are critical for Apolipoprotein AI downstream enhancer activity in human HepG2 cells
The factors that bind to the hepatic-specific human apolipoprotein AI ( apoAI) 48-bp downstream enhancer (DSE) were identified and characterized by electrophoretic mobility shift assays. A significant homology was shown between the histone 4 ( H4) promoters and the hepatic-specific human apoAI DSE a...
Gespeichert in:
| Veröffentlicht in: | Gene 2003-12, Vol.323, p.31-42 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 42 |
|---|---|
| container_issue | |
| container_start_page | 31 |
| container_title | Gene |
| container_volume | 323 |
| creator | Ivanov, Gleb S. Kater, Jessie M. Jha, Shivkumar H. Stutius, Erica A. Sabharwal, Ravleen Tricarico, Marisa D. Ginsburg, Geoffrey S. Ozer, Josef S. |
| description | The factors that bind to the hepatic-specific human
apolipoprotein AI (
apoAI) 48-bp downstream enhancer (DSE) were identified and characterized by electrophoretic mobility shift assays. A significant homology was shown between the
histone 4 (
H4) promoters and the hepatic-specific human
apoAI DSE at Sp1 and H4TF2 binding sites. Human HepG2 nuclear extracts were used to form four specific complexes with the DSE (referred to as apoAI DSE-1, -2, -3, and -4). The apoAI DSE-1 and -2 complexes showed similar binding specificity to the Sp/H4TF1 consensus site within the
apoAI DSE. The apoAI DSE-1 complex was predominantly recognized by anti-Sp1 and Sp3 sera in gel shift assays, indicating that the DSE was recognized by multiple Sp family members. Nuclear extracts that were prepared from retinoic acid treated HepG2 cells showed increased levels of Sp factors in gel shift and Western blot assays. The apoAI DSE-2 complex was identified as H4TF1 and formed in the absence of magnesium chloride. The apoAI DSE-3 complex bound to a consensus GATA element within the DSE that was recognized by recombinant human GATA-6 as well. The apoAI DSE-3 complex was completely disrupted by a GATA-4 antibody in EMSA. GATA-4 and -6 were detected in nuclear extracts prepared from retinoic acid treated HepG2 cells using Western blot assays. The highest apoAI DSE-3 levels were observed with retinoic acid treated HepG2 cell nuclear extracts in EMSA. ApoAI DSE-4 is a multi-factor complex that includes an Sp/H4TF1 factor and either H4TF2 or apoAI DSE-3. Because
apoAI DSE mutations revealed transcription defects in transient transfection assays, we conclude that the entire DSE sequence is required for full
apoAI transcriptional activity in HepG2 cells. |
| doi_str_mv | 10.1016/j.gene.2003.08.014 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71488523</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0378111903008643</els_id><sourcerecordid>71488523</sourcerecordid><originalsourceid>FETCH-LOGICAL-c383t-d767eef9ff51cae19b18485fb08f31165f7071f396864d3c5c195bc1b6fd48ca3</originalsourceid><addsrcrecordid>eNqFkUFr3DAQhUVoSbZJ_kAPRafe7Ggsy5KhFxPaTSDQQ9OzkOVRV4ttuZI3Jf--Wnaht2YuA8P3HsN7hHwEVgKD5m5f_sIZy4oxXjJVMqgvyAaUbIt8Ue_IhnGpCgBor8iHlPYsjxDVJbmCuhGtknJDdj8WauaBbrvnjjpj1xATNRGpjX711ozUhUi7JYx-CUsMK_qZdo90CH_mtEY0E8V5Z2aLkWa1f_HrK83I7jCZmT7gsq2oxXFMN-S9M2PC2_O-Jj-_fX2-fyievm8f77unwnLF12KQjUR0rXMCrEFoe1C1Eq5nynGARjjJJDjeNqqpB26FhVb0FvrGDbWyhl-Tzyff_OzvA6ZVTz4dPzAzhkPSEmqlRMXfBEEqVTc1ZLA6gTaGlCI6vUQ_mfiqgeljEXqvj0XoYxGaKZ2LyKJPZ_dDP-HwT3JOPgNfTgDmMF48Rp2sx5zj4CPaVQ_B_8__L-VEmZY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17884641</pqid></control><display><type>article</type><title>Sp and GATA factors are critical for Apolipoprotein AI downstream enhancer activity in human HepG2 cells</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Ivanov, Gleb S. ; Kater, Jessie M. ; Jha, Shivkumar H. ; Stutius, Erica A. ; Sabharwal, Ravleen ; Tricarico, Marisa D. ; Ginsburg, Geoffrey S. ; Ozer, Josef S.</creator><creatorcontrib>Ivanov, Gleb S. ; Kater, Jessie M. ; Jha, Shivkumar H. ; Stutius, Erica A. ; Sabharwal, Ravleen ; Tricarico, Marisa D. ; Ginsburg, Geoffrey S. ; Ozer, Josef S.</creatorcontrib><description>The factors that bind to the hepatic-specific human
apolipoprotein AI (
apoAI) 48-bp downstream enhancer (DSE) were identified and characterized by electrophoretic mobility shift assays. A significant homology was shown between the
histone 4 (
H4) promoters and the hepatic-specific human
apoAI DSE at Sp1 and H4TF2 binding sites. Human HepG2 nuclear extracts were used to form four specific complexes with the DSE (referred to as apoAI DSE-1, -2, -3, and -4). The apoAI DSE-1 and -2 complexes showed similar binding specificity to the Sp/H4TF1 consensus site within the
apoAI DSE. The apoAI DSE-1 complex was predominantly recognized by anti-Sp1 and Sp3 sera in gel shift assays, indicating that the DSE was recognized by multiple Sp family members. Nuclear extracts that were prepared from retinoic acid treated HepG2 cells showed increased levels of Sp factors in gel shift and Western blot assays. The apoAI DSE-2 complex was identified as H4TF1 and formed in the absence of magnesium chloride. The apoAI DSE-3 complex bound to a consensus GATA element within the DSE that was recognized by recombinant human GATA-6 as well. The apoAI DSE-3 complex was completely disrupted by a GATA-4 antibody in EMSA. GATA-4 and -6 were detected in nuclear extracts prepared from retinoic acid treated HepG2 cells using Western blot assays. The highest apoAI DSE-3 levels were observed with retinoic acid treated HepG2 cell nuclear extracts in EMSA. ApoAI DSE-4 is a multi-factor complex that includes an Sp/H4TF1 factor and either H4TF2 or apoAI DSE-3. Because
apoAI DSE mutations revealed transcription defects in transient transfection assays, we conclude that the entire DSE sequence is required for full
apoAI transcriptional activity in HepG2 cells.</description><identifier>ISSN: 0378-1119</identifier><identifier>EISSN: 1879-0038</identifier><identifier>DOI: 10.1016/j.gene.2003.08.014</identifier><identifier>PMID: 14659877</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>apoAIV ; apoCIII ; Apolipoprotein A-I - genetics ; Base Sequence ; Binding Sites - genetics ; Cell Line, Tumor ; DNA-Binding Proteins - metabolism ; Electrophoretic Mobility Shift Assay ; Enhancer Elements, Genetic - genetics ; GATA4 Transcription Factor ; GATA6 Transcription Factor ; Gene Expression Regulation, Neoplastic ; H4TF ; HDL ; HiNF ; Humans ; Liver - metabolism ; Molecular Sequence Data ; Oligonucleotides - genetics ; Oligonucleotides - metabolism ; Protein Binding ; Retinoic acid ; Sp1 Transcription Factor - metabolism ; Transcription Factors - metabolism ; Transfection</subject><ispartof>Gene, 2003-12, Vol.323, p.31-42</ispartof><rights>2003 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c383t-d767eef9ff51cae19b18485fb08f31165f7071f396864d3c5c195bc1b6fd48ca3</citedby><cites>FETCH-LOGICAL-c383t-d767eef9ff51cae19b18485fb08f31165f7071f396864d3c5c195bc1b6fd48ca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0378111903008643$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14659877$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ivanov, Gleb S.</creatorcontrib><creatorcontrib>Kater, Jessie M.</creatorcontrib><creatorcontrib>Jha, Shivkumar H.</creatorcontrib><creatorcontrib>Stutius, Erica A.</creatorcontrib><creatorcontrib>Sabharwal, Ravleen</creatorcontrib><creatorcontrib>Tricarico, Marisa D.</creatorcontrib><creatorcontrib>Ginsburg, Geoffrey S.</creatorcontrib><creatorcontrib>Ozer, Josef S.</creatorcontrib><title>Sp and GATA factors are critical for Apolipoprotein AI downstream enhancer activity in human HepG2 cells</title><title>Gene</title><addtitle>Gene</addtitle><description>The factors that bind to the hepatic-specific human
apolipoprotein AI (
apoAI) 48-bp downstream enhancer (DSE) were identified and characterized by electrophoretic mobility shift assays. A significant homology was shown between the
histone 4 (
H4) promoters and the hepatic-specific human
apoAI DSE at Sp1 and H4TF2 binding sites. Human HepG2 nuclear extracts were used to form four specific complexes with the DSE (referred to as apoAI DSE-1, -2, -3, and -4). The apoAI DSE-1 and -2 complexes showed similar binding specificity to the Sp/H4TF1 consensus site within the
apoAI DSE. The apoAI DSE-1 complex was predominantly recognized by anti-Sp1 and Sp3 sera in gel shift assays, indicating that the DSE was recognized by multiple Sp family members. Nuclear extracts that were prepared from retinoic acid treated HepG2 cells showed increased levels of Sp factors in gel shift and Western blot assays. The apoAI DSE-2 complex was identified as H4TF1 and formed in the absence of magnesium chloride. The apoAI DSE-3 complex bound to a consensus GATA element within the DSE that was recognized by recombinant human GATA-6 as well. The apoAI DSE-3 complex was completely disrupted by a GATA-4 antibody in EMSA. GATA-4 and -6 were detected in nuclear extracts prepared from retinoic acid treated HepG2 cells using Western blot assays. The highest apoAI DSE-3 levels were observed with retinoic acid treated HepG2 cell nuclear extracts in EMSA. ApoAI DSE-4 is a multi-factor complex that includes an Sp/H4TF1 factor and either H4TF2 or apoAI DSE-3. Because
apoAI DSE mutations revealed transcription defects in transient transfection assays, we conclude that the entire DSE sequence is required for full
apoAI transcriptional activity in HepG2 cells.</description><subject>apoAIV</subject><subject>apoCIII</subject><subject>Apolipoprotein A-I - genetics</subject><subject>Base Sequence</subject><subject>Binding Sites - genetics</subject><subject>Cell Line, Tumor</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>Enhancer Elements, Genetic - genetics</subject><subject>GATA4 Transcription Factor</subject><subject>GATA6 Transcription Factor</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>H4TF</subject><subject>HDL</subject><subject>HiNF</subject><subject>Humans</subject><subject>Liver - metabolism</subject><subject>Molecular Sequence Data</subject><subject>Oligonucleotides - genetics</subject><subject>Oligonucleotides - metabolism</subject><subject>Protein Binding</subject><subject>Retinoic acid</subject><subject>Sp1 Transcription Factor - metabolism</subject><subject>Transcription Factors - metabolism</subject><subject>Transfection</subject><issn>0378-1119</issn><issn>1879-0038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFr3DAQhUVoSbZJ_kAPRafe7Ggsy5KhFxPaTSDQQ9OzkOVRV4ttuZI3Jf--Wnaht2YuA8P3HsN7hHwEVgKD5m5f_sIZy4oxXjJVMqgvyAaUbIt8Ue_IhnGpCgBor8iHlPYsjxDVJbmCuhGtknJDdj8WauaBbrvnjjpj1xATNRGpjX711ozUhUi7JYx-CUsMK_qZdo90CH_mtEY0E8V5Z2aLkWa1f_HrK83I7jCZmT7gsq2oxXFMN-S9M2PC2_O-Jj-_fX2-fyievm8f77unwnLF12KQjUR0rXMCrEFoe1C1Eq5nynGARjjJJDjeNqqpB26FhVb0FvrGDbWyhl-Tzyff_OzvA6ZVTz4dPzAzhkPSEmqlRMXfBEEqVTc1ZLA6gTaGlCI6vUQ_mfiqgeljEXqvj0XoYxGaKZ2LyKJPZ_dDP-HwT3JOPgNfTgDmMF48Rp2sx5zj4CPaVQ_B_8__L-VEmZY</recordid><startdate>20031224</startdate><enddate>20031224</enddate><creator>Ivanov, Gleb S.</creator><creator>Kater, Jessie M.</creator><creator>Jha, Shivkumar H.</creator><creator>Stutius, Erica A.</creator><creator>Sabharwal, Ravleen</creator><creator>Tricarico, Marisa D.</creator><creator>Ginsburg, Geoffrey S.</creator><creator>Ozer, Josef S.</creator><general>Elsevier B.V</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>7TM</scope><scope>7X8</scope></search><sort><creationdate>20031224</creationdate><title>Sp and GATA factors are critical for Apolipoprotein AI downstream enhancer activity in human HepG2 cells</title><author>Ivanov, Gleb S. ; Kater, Jessie M. ; Jha, Shivkumar H. ; Stutius, Erica A. ; Sabharwal, Ravleen ; Tricarico, Marisa D. ; Ginsburg, Geoffrey S. ; Ozer, Josef S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c383t-d767eef9ff51cae19b18485fb08f31165f7071f396864d3c5c195bc1b6fd48ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>apoAIV</topic><topic>apoCIII</topic><topic>Apolipoprotein A-I - genetics</topic><topic>Base Sequence</topic><topic>Binding Sites - genetics</topic><topic>Cell Line, Tumor</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Electrophoretic Mobility Shift Assay</topic><topic>Enhancer Elements, Genetic - genetics</topic><topic>GATA4 Transcription Factor</topic><topic>GATA6 Transcription Factor</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>H4TF</topic><topic>HDL</topic><topic>HiNF</topic><topic>Humans</topic><topic>Liver - metabolism</topic><topic>Molecular Sequence Data</topic><topic>Oligonucleotides - genetics</topic><topic>Oligonucleotides - metabolism</topic><topic>Protein Binding</topic><topic>Retinoic acid</topic><topic>Sp1 Transcription Factor - metabolism</topic><topic>Transcription Factors - metabolism</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ivanov, Gleb S.</creatorcontrib><creatorcontrib>Kater, Jessie M.</creatorcontrib><creatorcontrib>Jha, Shivkumar H.</creatorcontrib><creatorcontrib>Stutius, Erica A.</creatorcontrib><creatorcontrib>Sabharwal, Ravleen</creatorcontrib><creatorcontrib>Tricarico, Marisa D.</creatorcontrib><creatorcontrib>Ginsburg, Geoffrey S.</creatorcontrib><creatorcontrib>Ozer, Josef S.</creatorcontrib><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>Gene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ivanov, Gleb S.</au><au>Kater, Jessie M.</au><au>Jha, Shivkumar H.</au><au>Stutius, Erica A.</au><au>Sabharwal, Ravleen</au><au>Tricarico, Marisa D.</au><au>Ginsburg, Geoffrey S.</au><au>Ozer, Josef S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sp and GATA factors are critical for Apolipoprotein AI downstream enhancer activity in human HepG2 cells</atitle><jtitle>Gene</jtitle><addtitle>Gene</addtitle><date>2003-12-24</date><risdate>2003</risdate><volume>323</volume><spage>31</spage><epage>42</epage><pages>31-42</pages><issn>0378-1119</issn><eissn>1879-0038</eissn><abstract>The factors that bind to the hepatic-specific human
apolipoprotein AI (
apoAI) 48-bp downstream enhancer (DSE) were identified and characterized by electrophoretic mobility shift assays. A significant homology was shown between the
histone 4 (
H4) promoters and the hepatic-specific human
apoAI DSE at Sp1 and H4TF2 binding sites. Human HepG2 nuclear extracts were used to form four specific complexes with the DSE (referred to as apoAI DSE-1, -2, -3, and -4). The apoAI DSE-1 and -2 complexes showed similar binding specificity to the Sp/H4TF1 consensus site within the
apoAI DSE. The apoAI DSE-1 complex was predominantly recognized by anti-Sp1 and Sp3 sera in gel shift assays, indicating that the DSE was recognized by multiple Sp family members. Nuclear extracts that were prepared from retinoic acid treated HepG2 cells showed increased levels of Sp factors in gel shift and Western blot assays. The apoAI DSE-2 complex was identified as H4TF1 and formed in the absence of magnesium chloride. The apoAI DSE-3 complex bound to a consensus GATA element within the DSE that was recognized by recombinant human GATA-6 as well. The apoAI DSE-3 complex was completely disrupted by a GATA-4 antibody in EMSA. GATA-4 and -6 were detected in nuclear extracts prepared from retinoic acid treated HepG2 cells using Western blot assays. The highest apoAI DSE-3 levels were observed with retinoic acid treated HepG2 cell nuclear extracts in EMSA. ApoAI DSE-4 is a multi-factor complex that includes an Sp/H4TF1 factor and either H4TF2 or apoAI DSE-3. Because
apoAI DSE mutations revealed transcription defects in transient transfection assays, we conclude that the entire DSE sequence is required for full
apoAI transcriptional activity in HepG2 cells.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>14659877</pmid><doi>10.1016/j.gene.2003.08.014</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0378-1119 |
| ispartof | Gene, 2003-12, Vol.323, p.31-42 |
| issn | 0378-1119 1879-0038 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71488523 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | apoAIV apoCIII Apolipoprotein A-I - genetics Base Sequence Binding Sites - genetics Cell Line, Tumor DNA-Binding Proteins - metabolism Electrophoretic Mobility Shift Assay Enhancer Elements, Genetic - genetics GATA4 Transcription Factor GATA6 Transcription Factor Gene Expression Regulation, Neoplastic H4TF HDL HiNF Humans Liver - metabolism Molecular Sequence Data Oligonucleotides - genetics Oligonucleotides - metabolism Protein Binding Retinoic acid Sp1 Transcription Factor - metabolism Transcription Factors - metabolism Transfection |
| title | Sp and GATA factors are critical for Apolipoprotein AI downstream enhancer activity in human HepG2 cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T17%3A30%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Sp%20and%20GATA%20factors%20are%20critical%20for%20Apolipoprotein%20AI%20downstream%20enhancer%20activity%20in%20human%20HepG2%20cells&rft.jtitle=Gene&rft.au=Ivanov,%20Gleb%20S.&rft.date=2003-12-24&rft.volume=323&rft.spage=31&rft.epage=42&rft.pages=31-42&rft.issn=0378-1119&rft.eissn=1879-0038&rft_id=info:doi/10.1016/j.gene.2003.08.014&rft_dat=%3Cproquest_cross%3E71488523%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=17884641&rft_id=info:pmid/14659877&rft_els_id=S0378111903008643&rfr_iscdi=true |