HIC1 interacts with a specific subunit of SWI/SNF complexes, ARID1A/BAF250A
HIC1, a tumor suppressor gene epigenetically silenced in many human cancers encodes a transcriptional repressor involved in regulatory loops modulating p53-dependent and E2F1-dependent cell survival and stress responses. HIC1 is also implicated in growth control since it recruits BRG1, one of the tw...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2009-08, Vol.385 (4), p.586-590 |
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| creator | Van Rechem, Capucine Boulay, Gaylor Leprince, Dominique |
| description | HIC1, a tumor suppressor gene epigenetically silenced in many human cancers encodes a transcriptional repressor involved in regulatory loops modulating p53-dependent and E2F1-dependent cell survival and stress responses. HIC1 is also implicated in growth control since it recruits BRG1, one of the two alternative ATPases (BRM or BRG1) of SWI/SNF chromatin-remodeling complexes to repress transcription of
E2F1 in quiescent fibroblasts. Here, through yeast two-hybrid screening, we identify ARID1A/BAF250A, as a new HIC1 partner. ARID1A/BAF250A is one of the two mutually exclusive ARID1-containing subunits of SWI/SNF complexes which define subsets of complexes endowed with anti-proliferative properties. Co-immunoprecipitation assays in WI38 fibroblasts and in BRG1−/− SW13 cells showed that endogenous HIC1 and ARID1A proteins interact in a BRG1-dependent manner. Furthermore, we demonstrate that HIC1 does not interact with BRM. Finally, sequential chromatin immunoprecipitation (ChIP-reChIP) experiments demonstrated that HIC1 represses
E2F1 through the recruitment of anti-proliferative SWI/SNF complexes containing ARID1A. |
| doi_str_mv | 10.1016/j.bbrc.2009.05.115 |
| format | Article |
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E2F1 in quiescent fibroblasts. Here, through yeast two-hybrid screening, we identify ARID1A/BAF250A, as a new HIC1 partner. ARID1A/BAF250A is one of the two mutually exclusive ARID1-containing subunits of SWI/SNF complexes which define subsets of complexes endowed with anti-proliferative properties. Co-immunoprecipitation assays in WI38 fibroblasts and in BRG1−/− SW13 cells showed that endogenous HIC1 and ARID1A proteins interact in a BRG1-dependent manner. Furthermore, we demonstrate that HIC1 does not interact with BRM. Finally, sequential chromatin immunoprecipitation (ChIP-reChIP) experiments demonstrated that HIC1 represses
E2F1 through the recruitment of anti-proliferative SWI/SNF complexes containing ARID1A.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2009.05.115</identifier><identifier>PMID: 19486893</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>17p13.3 ; 60 APPLIED LIFE SCIENCES ; ARID1A ; BAF250A ; BRG1 ; BTB/POZ ; Cell Line ; CHROMATIN ; Chromatin Immunoprecipitation ; Down-Regulation ; E2F1 Transcription Factor - genetics ; FIBROBLASTS ; Gene Expression Regulation, Neoplastic ; GENES ; HIC1 ; Humans ; HYBRIDIZATION ; Kruppel-Like Transcription Factors - genetics ; Kruppel-Like Transcription Factors - metabolism ; NEOPLASMS ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Protein Subunits - genetics ; Protein Subunits - metabolism ; PROTEINS ; SCREENING ; SWI/SNF complexes ; TRANSCRIPTION ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transcriptional repression ; Tumor suppressor genes ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Two-Hybrid System Techniques ; YEASTS</subject><ispartof>Biochemical and biophysical research communications, 2009-08, Vol.385 (4), p.586-590</ispartof><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-27215c8740593570a5e8aa1c4c7518a1bfee4aff1c07f4adec61ef5cee1a33d93</citedby><cites>FETCH-LOGICAL-c413t-27215c8740593570a5e8aa1c4c7518a1bfee4aff1c07f4adec61ef5cee1a33d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X0901064X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19486893$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22199757$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Van Rechem, Capucine</creatorcontrib><creatorcontrib>Boulay, Gaylor</creatorcontrib><creatorcontrib>Leprince, Dominique</creatorcontrib><title>HIC1 interacts with a specific subunit of SWI/SNF complexes, ARID1A/BAF250A</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>HIC1, a tumor suppressor gene epigenetically silenced in many human cancers encodes a transcriptional repressor involved in regulatory loops modulating p53-dependent and E2F1-dependent cell survival and stress responses. HIC1 is also implicated in growth control since it recruits BRG1, one of the two alternative ATPases (BRM or BRG1) of SWI/SNF chromatin-remodeling complexes to repress transcription of
E2F1 in quiescent fibroblasts. Here, through yeast two-hybrid screening, we identify ARID1A/BAF250A, as a new HIC1 partner. ARID1A/BAF250A is one of the two mutually exclusive ARID1-containing subunits of SWI/SNF complexes which define subsets of complexes endowed with anti-proliferative properties. Co-immunoprecipitation assays in WI38 fibroblasts and in BRG1−/− SW13 cells showed that endogenous HIC1 and ARID1A proteins interact in a BRG1-dependent manner. Furthermore, we demonstrate that HIC1 does not interact with BRM. Finally, sequential chromatin immunoprecipitation (ChIP-reChIP) experiments demonstrated that HIC1 represses
E2F1 through the recruitment of anti-proliferative SWI/SNF complexes containing ARID1A.</description><subject>17p13.3</subject><subject>60 APPLIED LIFE SCIENCES</subject><subject>ARID1A</subject><subject>BAF250A</subject><subject>BRG1</subject><subject>BTB/POZ</subject><subject>Cell Line</subject><subject>CHROMATIN</subject><subject>Chromatin Immunoprecipitation</subject><subject>Down-Regulation</subject><subject>E2F1 Transcription Factor - genetics</subject><subject>FIBROBLASTS</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>GENES</subject><subject>HIC1</subject><subject>Humans</subject><subject>HYBRIDIZATION</subject><subject>Kruppel-Like Transcription Factors - genetics</subject><subject>Kruppel-Like Transcription Factors - metabolism</subject><subject>NEOPLASMS</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Protein Subunits - genetics</subject><subject>Protein Subunits - metabolism</subject><subject>PROTEINS</subject><subject>SCREENING</subject><subject>SWI/SNF complexes</subject><subject>TRANSCRIPTION</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transcriptional repression</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Two-Hybrid System Techniques</subject><subject>YEASTS</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUGL1EAQhRtR3HH1D3iQgODJZKo63Z1p8BLHHXdwUXAVvTWdSoXtYSYZ04m6_96EGfCmp7p878GrT4jnCBkCmuUuq6qeMglgM9AZon4gFggWUomgHooFAJhUWvx-IZ7EuANAVMY-Fhdo1cqsbL4QH663a0xCO3DvaYjJrzDcJT6JR6bQBEriWI1tGJKuSW6_bZe3HzcJdYfjnn9zfJ2Un7fvsFy-LTdSQ_lUPGr8PvKz870UXzdXX9bX6c2n99t1eZOSwnxIZSFR06pQoG2uC_CaV94jKSo0rjxWDbPyTYMERaN8zWSQG03M6PO8tvmleHnq7eIQXKQwMN1R17ZMg5MSrS10MVGvTtSx736MHAd3CJF4v_ctd2N0plAIuTT_BSUYo0yuJ1CeQOq7GHtu3LEPB9_fOwQ3G3E7NxtxsxEH2k1GptCLc_tYHbj-GzkrmIA3J4Cnl_0M3M-LuCWuQz8Pqrvwr_4_RK-YyA</recordid><startdate>20090807</startdate><enddate>20090807</enddate><creator>Van Rechem, Capucine</creator><creator>Boulay, Gaylor</creator><creator>Leprince, Dominique</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>7TO</scope><scope>H94</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20090807</creationdate><title>HIC1 interacts with a specific subunit of SWI/SNF complexes, ARID1A/BAF250A</title><author>Van Rechem, Capucine ; Boulay, Gaylor ; Leprince, Dominique</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-27215c8740593570a5e8aa1c4c7518a1bfee4aff1c07f4adec61ef5cee1a33d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>17p13.3</topic><topic>60 APPLIED LIFE SCIENCES</topic><topic>ARID1A</topic><topic>BAF250A</topic><topic>BRG1</topic><topic>BTB/POZ</topic><topic>Cell Line</topic><topic>CHROMATIN</topic><topic>Chromatin Immunoprecipitation</topic><topic>Down-Regulation</topic><topic>E2F1 Transcription Factor - genetics</topic><topic>FIBROBLASTS</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>GENES</topic><topic>HIC1</topic><topic>Humans</topic><topic>HYBRIDIZATION</topic><topic>Kruppel-Like Transcription Factors - genetics</topic><topic>Kruppel-Like Transcription Factors - metabolism</topic><topic>NEOPLASMS</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Protein Subunits - genetics</topic><topic>Protein Subunits - metabolism</topic><topic>PROTEINS</topic><topic>SCREENING</topic><topic>SWI/SNF complexes</topic><topic>TRANSCRIPTION</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transcriptional repression</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>Two-Hybrid System Techniques</topic><topic>YEASTS</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Van Rechem, Capucine</creatorcontrib><creatorcontrib>Boulay, Gaylor</creatorcontrib><creatorcontrib>Leprince, Dominique</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Van Rechem, Capucine</au><au>Boulay, Gaylor</au><au>Leprince, Dominique</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HIC1 interacts with a specific subunit of SWI/SNF complexes, ARID1A/BAF250A</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2009-08-07</date><risdate>2009</risdate><volume>385</volume><issue>4</issue><spage>586</spage><epage>590</epage><pages>586-590</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>HIC1, a tumor suppressor gene epigenetically silenced in many human cancers encodes a transcriptional repressor involved in regulatory loops modulating p53-dependent and E2F1-dependent cell survival and stress responses. HIC1 is also implicated in growth control since it recruits BRG1, one of the two alternative ATPases (BRM or BRG1) of SWI/SNF chromatin-remodeling complexes to repress transcription of
E2F1 in quiescent fibroblasts. Here, through yeast two-hybrid screening, we identify ARID1A/BAF250A, as a new HIC1 partner. ARID1A/BAF250A is one of the two mutually exclusive ARID1-containing subunits of SWI/SNF complexes which define subsets of complexes endowed with anti-proliferative properties. Co-immunoprecipitation assays in WI38 fibroblasts and in BRG1−/− SW13 cells showed that endogenous HIC1 and ARID1A proteins interact in a BRG1-dependent manner. Furthermore, we demonstrate that HIC1 does not interact with BRM. Finally, sequential chromatin immunoprecipitation (ChIP-reChIP) experiments demonstrated that HIC1 represses
E2F1 through the recruitment of anti-proliferative SWI/SNF complexes containing ARID1A.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19486893</pmid><doi>10.1016/j.bbrc.2009.05.115</doi><tpages>5</tpages></addata></record> |
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| subjects | 17p13.3 60 APPLIED LIFE SCIENCES ARID1A BAF250A BRG1 BTB/POZ Cell Line CHROMATIN Chromatin Immunoprecipitation Down-Regulation E2F1 Transcription Factor - genetics FIBROBLASTS Gene Expression Regulation, Neoplastic GENES HIC1 Humans HYBRIDIZATION Kruppel-Like Transcription Factors - genetics Kruppel-Like Transcription Factors - metabolism NEOPLASMS Nuclear Proteins - genetics Nuclear Proteins - metabolism Protein Subunits - genetics Protein Subunits - metabolism PROTEINS SCREENING SWI/SNF complexes TRANSCRIPTION Transcription Factors - genetics Transcription Factors - metabolism Transcriptional repression Tumor suppressor genes Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Two-Hybrid System Techniques YEASTS |
| title | HIC1 interacts with a specific subunit of SWI/SNF complexes, ARID1A/BAF250A |
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