Brain-specific angiogenesis inhibitor 2 regulates VEGF through GABP that acts as a transcriptional repressor
Previously, we reported that decreased brain-specific angiogenesis inhibitor 2 (BAI2) induced increased VEGF expression. The regulatory mechanisms for this process are not understood. Here we show that GA-binding protein gamma (GABPγ) associates with the cytoplasmic domain of BAI2, and GABPα/γ or GA...
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| Veröffentlicht in: | FEBS letters 2006-01, Vol.580 (2), p.669-676 |
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| creator | Jeong, Byung Chul Kim, Mi-Young Lee, Ji Hee Kee, Hae Jin Kho, Dhong Hyo Han, Kae Eun Qian, Yong Ri Kim, Jong-Keun Kim, Kyung Keun |
| description | Previously, we reported that decreased brain-specific angiogenesis inhibitor 2 (BAI2) induced increased VEGF expression. The regulatory mechanisms for this process are not understood. Here we show that GA-binding protein gamma (GABPγ) associates with the cytoplasmic domain of BAI2, and GABPα/γ or GABPα/β works as a transcriptional repressor of VEGF in SHSY5Y cells. Transcriptional activity of wild-type VEGF promoter was significantly increased in anti-sense BAI2-transfected cells, but not that of VEGF promoter harboring mutated GABP sites. In in vivo focal cerebral ischemia model, the decrease in BAI2 accompanied by decreased GABPα and GABPγ elicited increased VEGF expression before the onset of HIF-1α. Our results point out that BAI2 controls VEGF transcription through GABP under normal conditions and cerebral ischemia. |
| doi_str_mv | 10.1016/j.febslet.2005.12.086 |
| format | Article |
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The regulatory mechanisms for this process are not understood. Here we show that GA-binding protein gamma (GABPγ) associates with the cytoplasmic domain of BAI2, and GABPα/γ or GABPα/β works as a transcriptional repressor of VEGF in SHSY5Y cells. Transcriptional activity of wild-type VEGF promoter was significantly increased in anti-sense BAI2-transfected cells, but not that of VEGF promoter harboring mutated GABP sites. In in vivo focal cerebral ischemia model, the decrease in BAI2 accompanied by decreased GABPα and GABPγ elicited increased VEGF expression before the onset of HIF-1α. Our results point out that BAI2 controls VEGF transcription through GABP under normal conditions and cerebral ischemia.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2005.12.086</identifier><identifier>PMID: 16412436</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Animals ; BAI2 ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain-specific angiogenesis inhibitor 2 ; Cell Line ; Cerebral ischemia ; ChIP ; chromatin immunoprecipitation ; CV-1 cells ; electrophoretic mobility shift assay ; EMSA ; GA-binding protein ; GA-Binding Protein Transcription Factor - genetics ; GA-Binding Protein Transcription Factor - metabolism ; GABP ; Green monkey kidney epithelial cells ; Humans ; immunoprecipitation ; MCA ; Membrane Proteins ; Mice ; middle cerebral artery ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Protein Subunits - genetics ; Protein Subunits - metabolism ; Rats ; Rats, Sprague-Dawley ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; SDS–PAGE ; sodium dodecyl sulfate–polyacrylamide gel electrophoresis ; Transcription, Genetic ; Transcriptional repressor ; triphenyl tetrazolium chloride ; TTC ; Two-Hybrid System Techniques ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism ; VEGF</subject><ispartof>FEBS letters, 2006-01, Vol.580 (2), p.669-676</ispartof><rights>2005 Federation of European Biochemical Societies</rights><rights>FEBS Letters 580 (2006) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4591-44ee649e91ffe3a6f58fb91db5d3bc66c8eb38e43a39c98e6650170497512d7d3</citedby><cites>FETCH-LOGICAL-c4591-44ee649e91ffe3a6f58fb91db5d3bc66c8eb38e43a39c98e6650170497512d7d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.febslet.2005.12.086$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.febslet.2005.12.086$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,1417,1433,3550,27924,27925,45574,45575,45995,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16412436$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jeong, Byung Chul</creatorcontrib><creatorcontrib>Kim, Mi-Young</creatorcontrib><creatorcontrib>Lee, Ji Hee</creatorcontrib><creatorcontrib>Kee, Hae Jin</creatorcontrib><creatorcontrib>Kho, Dhong Hyo</creatorcontrib><creatorcontrib>Han, Kae Eun</creatorcontrib><creatorcontrib>Qian, Yong Ri</creatorcontrib><creatorcontrib>Kim, Jong-Keun</creatorcontrib><creatorcontrib>Kim, Kyung Keun</creatorcontrib><title>Brain-specific angiogenesis inhibitor 2 regulates VEGF through GABP that acts as a transcriptional repressor</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>Previously, we reported that decreased brain-specific angiogenesis inhibitor 2 (BAI2) induced increased VEGF expression. The regulatory mechanisms for this process are not understood. Here we show that GA-binding protein gamma (GABPγ) associates with the cytoplasmic domain of BAI2, and GABPα/γ or GABPα/β works as a transcriptional repressor of VEGF in SHSY5Y cells. Transcriptional activity of wild-type VEGF promoter was significantly increased in anti-sense BAI2-transfected cells, but not that of VEGF promoter harboring mutated GABP sites. In in vivo focal cerebral ischemia model, the decrease in BAI2 accompanied by decreased GABPα and GABPγ elicited increased VEGF expression before the onset of HIF-1α. Our results point out that BAI2 controls VEGF transcription through GABP under normal conditions and cerebral ischemia.</description><subject>Animals</subject><subject>BAI2</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain-specific angiogenesis inhibitor 2</subject><subject>Cell Line</subject><subject>Cerebral ischemia</subject><subject>ChIP</subject><subject>chromatin immunoprecipitation</subject><subject>CV-1 cells</subject><subject>electrophoretic mobility shift assay</subject><subject>EMSA</subject><subject>GA-binding protein</subject><subject>GA-Binding Protein Transcription Factor - genetics</subject><subject>GA-Binding Protein Transcription Factor - metabolism</subject><subject>GABP</subject><subject>Green monkey kidney epithelial cells</subject><subject>Humans</subject><subject>immunoprecipitation</subject><subject>MCA</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>middle cerebral artery</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Protein Subunits - genetics</subject><subject>Protein Subunits - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>SDS–PAGE</subject><subject>sodium dodecyl sulfate–polyacrylamide gel electrophoresis</subject><subject>Transcription, Genetic</subject><subject>Transcriptional repressor</subject><subject>triphenyl tetrazolium chloride</subject><subject>TTC</subject><subject>Two-Hybrid System Techniques</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>VEGF</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV1r2zAUhsXYWLNuP2FDV7uzq2N92LoaTUnSQWGDfdwKWT5OFBw7k-SO_vspJLDLFgTiwPO--ngI-QisBAbqZl_22MYBU1kxJkuoStaoV2QBTc0LLlTzmiwYA1HIWvMr8i7GPctzA_otuQIloBJcLciwDNaPRTyi87131I5bP21xxOgj9ePOtz5NgVY04HYebMJIf682a5p2YZq3O7q5XX7Pg03UuhSpzYumYMfogj8mP412yNFjwBin8J686e0Q8cNlvya_1qufd_fFw7fN17vbh8IJqaEQAlEJjRr6HrlVvWz6VkPXyo63TinXYMsbFNxy7XSDSkkGNRO6llB1dcevyedz7zFMf2aMyRx8dDgMdsRpjqZmqmFMiWdB0DXTtZYZlGfQhSnGgL05Bn-w4ckAMycfZm8uPszJh4HKZB859-lywNwesPufugjIwP0Z-OsHfHpZq1mvltWPk9yTW5YfL2uAXPXlXIX5ax89BhOdx9Fh5wO6ZLrJP3Pbf0H-tKU</recordid><startdate>20060123</startdate><enddate>20060123</enddate><creator>Jeong, Byung Chul</creator><creator>Kim, Mi-Young</creator><creator>Lee, Ji Hee</creator><creator>Kee, Hae Jin</creator><creator>Kho, Dhong Hyo</creator><creator>Han, Kae Eun</creator><creator>Qian, Yong Ri</creator><creator>Kim, Jong-Keun</creator><creator>Kim, Kyung Keun</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</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>7TK</scope><scope>7TM</scope><scope>7X8</scope></search><sort><creationdate>20060123</creationdate><title>Brain-specific angiogenesis inhibitor 2 regulates VEGF through GABP that acts as a transcriptional repressor</title><author>Jeong, Byung Chul ; Kim, Mi-Young ; Lee, Ji Hee ; Kee, Hae Jin ; Kho, Dhong Hyo ; Han, Kae Eun ; Qian, Yong Ri ; Kim, Jong-Keun ; Kim, Kyung Keun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4591-44ee649e91ffe3a6f58fb91db5d3bc66c8eb38e43a39c98e6650170497512d7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>BAI2</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Brain-specific angiogenesis inhibitor 2</topic><topic>Cell Line</topic><topic>Cerebral ischemia</topic><topic>ChIP</topic><topic>chromatin immunoprecipitation</topic><topic>CV-1 cells</topic><topic>electrophoretic mobility shift assay</topic><topic>EMSA</topic><topic>GA-binding protein</topic><topic>GA-Binding Protein Transcription Factor - genetics</topic><topic>GA-Binding Protein Transcription Factor - metabolism</topic><topic>GABP</topic><topic>Green monkey kidney epithelial cells</topic><topic>Humans</topic><topic>immunoprecipitation</topic><topic>MCA</topic><topic>Membrane Proteins</topic><topic>Mice</topic><topic>middle cerebral artery</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Protein Subunits - genetics</topic><topic>Protein Subunits - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>SDS–PAGE</topic><topic>sodium dodecyl sulfate–polyacrylamide gel electrophoresis</topic><topic>Transcription, Genetic</topic><topic>Transcriptional repressor</topic><topic>triphenyl tetrazolium chloride</topic><topic>TTC</topic><topic>Two-Hybrid System Techniques</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>VEGF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jeong, Byung Chul</creatorcontrib><creatorcontrib>Kim, Mi-Young</creatorcontrib><creatorcontrib>Lee, Ji Hee</creatorcontrib><creatorcontrib>Kee, Hae Jin</creatorcontrib><creatorcontrib>Kho, Dhong Hyo</creatorcontrib><creatorcontrib>Han, Kae Eun</creatorcontrib><creatorcontrib>Qian, Yong Ri</creatorcontrib><creatorcontrib>Kim, Jong-Keun</creatorcontrib><creatorcontrib>Kim, Kyung Keun</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jeong, Byung Chul</au><au>Kim, Mi-Young</au><au>Lee, Ji Hee</au><au>Kee, Hae Jin</au><au>Kho, Dhong Hyo</au><au>Han, Kae Eun</au><au>Qian, Yong Ri</au><au>Kim, Jong-Keun</au><au>Kim, Kyung Keun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain-specific angiogenesis inhibitor 2 regulates VEGF through GABP that acts as a transcriptional repressor</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2006-01-23</date><risdate>2006</risdate><volume>580</volume><issue>2</issue><spage>669</spage><epage>676</epage><pages>669-676</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>Previously, we reported that decreased brain-specific angiogenesis inhibitor 2 (BAI2) induced increased VEGF expression. The regulatory mechanisms for this process are not understood. Here we show that GA-binding protein gamma (GABPγ) associates with the cytoplasmic domain of BAI2, and GABPα/γ or GABPα/β works as a transcriptional repressor of VEGF in SHSY5Y cells. Transcriptional activity of wild-type VEGF promoter was significantly increased in anti-sense BAI2-transfected cells, but not that of VEGF promoter harboring mutated GABP sites. In in vivo focal cerebral ischemia model, the decrease in BAI2 accompanied by decreased GABPα and GABPγ elicited increased VEGF expression before the onset of HIF-1α. Our results point out that BAI2 controls VEGF transcription through GABP under normal conditions and cerebral ischemia.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>16412436</pmid><doi>10.1016/j.febslet.2005.12.086</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | FEBS letters, 2006-01, Vol.580 (2), p.669-676 |
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| subjects | Animals BAI2 Brain Ischemia - metabolism Brain Ischemia - pathology Brain-specific angiogenesis inhibitor 2 Cell Line Cerebral ischemia ChIP chromatin immunoprecipitation CV-1 cells electrophoretic mobility shift assay EMSA GA-binding protein GA-Binding Protein Transcription Factor - genetics GA-Binding Protein Transcription Factor - metabolism GABP Green monkey kidney epithelial cells Humans immunoprecipitation MCA Membrane Proteins Mice middle cerebral artery Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Protein Subunits - genetics Protein Subunits - metabolism Rats Rats, Sprague-Dawley Repressor Proteins - genetics Repressor Proteins - metabolism SDS–PAGE sodium dodecyl sulfate–polyacrylamide gel electrophoresis Transcription, Genetic Transcriptional repressor triphenyl tetrazolium chloride TTC Two-Hybrid System Techniques Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism VEGF |
| title | Brain-specific angiogenesis inhibitor 2 regulates VEGF through GABP that acts as a transcriptional repressor |
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