Promoter Analysis of Mouse Scn3a Gene and Regulation of the Promoter Activity by GC Box and CpG Methylation
Voltage-gated sodium channel α-subunit type III (Na v 1.3) is mainly expressed in the central nervous system and is associated with neurological disorders. The expression of mouse Scn3a product (Na v 1.3) mainly occurs in embryonic and early postnatal brain but not in adult brain. Here, we report fo...
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| Veröffentlicht in: | Journal of molecular neuroscience 2011-06, Vol.44 (2), p.115-121 |
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| creator | Deng, Guang-Fei Qin, Jia-Ming Sun, Xun-Sha Kuang, Zu-Ying Su, Tao Zhao, Qi-Hua Shi, Yi-Wu Liu, Xiao-Rong Yu, Mei-Juan Yi, Yong-Hong Liao, Wei-Ping Long, Yue-Sheng |
| description | Voltage-gated sodium channel α-subunit type III (Na
v
1.3) is mainly expressed in the central nervous system and is associated with neurological disorders. The expression of mouse
Scn3a
product (Na
v
1.3) mainly occurs in embryonic and early postnatal brain but not in adult brain. Here, we report for the first time the identification and characterization of the mouse
Scn3a
gene promoter region and regulation of the promoter activity by GC box and CpG methylation. Luciferase assay showed that the promoter region F1.2 (nt −1,049 to +157) had significantly higher activity in PC12 cells, comparing with that in SH-SY5Y cells and HEK293 cells. A stepwise 5′ truncation of the promoter region found that the minimal functional promoter located within the region nt −168 to +157. Deletion of a GC box (nt −254 to −258) in the mouse
Scn3a
promoter decreased the promoter activity. CpG methylation of the F1.2 without the GC box completely repressed the promoter activity, suggesting that the GC box is a critical element in the CpG-methylated
Scn3a
promoter. These results suggest that the GC box and CpG methylation might play important roles in regulating mouse
Scn3a
gene expression. |
| doi_str_mv | 10.1007/s12031-011-9492-8 |
| format | Article |
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v
1.3) is mainly expressed in the central nervous system and is associated with neurological disorders. The expression of mouse
Scn3a
product (Na
v
1.3) mainly occurs in embryonic and early postnatal brain but not in adult brain. Here, we report for the first time the identification and characterization of the mouse
Scn3a
gene promoter region and regulation of the promoter activity by GC box and CpG methylation. Luciferase assay showed that the promoter region F1.2 (nt −1,049 to +157) had significantly higher activity in PC12 cells, comparing with that in SH-SY5Y cells and HEK293 cells. A stepwise 5′ truncation of the promoter region found that the minimal functional promoter located within the region nt −168 to +157. Deletion of a GC box (nt −254 to −258) in the mouse
Scn3a
promoter decreased the promoter activity. CpG methylation of the F1.2 without the GC box completely repressed the promoter activity, suggesting that the GC box is a critical element in the CpG-methylated
Scn3a
promoter. These results suggest that the GC box and CpG methylation might play important roles in regulating mouse
Scn3a
gene expression.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-011-9492-8</identifier><identifier>PMID: 21271300</identifier><language>eng</language><publisher>New York: Humana Press Inc</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Line, Tumor ; Cloning ; CpG Islands ; Dinucleoside Phosphates - metabolism ; DNA Methylation ; Gene expression ; Gene Expression Regulation ; Humans ; Mice ; Mutagenesis, Site-Directed ; NAV1.3 Voltage-Gated Sodium Channel ; Nervous system ; Neurochemistry ; Neurology ; Neurosciences ; Promoter Regions, Genetic - genetics ; Proteomics ; Sodium ; Sodium Channels - genetics</subject><ispartof>Journal of molecular neuroscience, 2011-06, Vol.44 (2), p.115-121</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-d5c9a680a05f7a07d458e284d0168fd42b3f6a7e730875995e0fa2c1d2efefd93</citedby><cites>FETCH-LOGICAL-c370t-d5c9a680a05f7a07d458e284d0168fd42b3f6a7e730875995e0fa2c1d2efefd93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-011-9492-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-011-9492-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21271300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deng, Guang-Fei</creatorcontrib><creatorcontrib>Qin, Jia-Ming</creatorcontrib><creatorcontrib>Sun, Xun-Sha</creatorcontrib><creatorcontrib>Kuang, Zu-Ying</creatorcontrib><creatorcontrib>Su, Tao</creatorcontrib><creatorcontrib>Zhao, Qi-Hua</creatorcontrib><creatorcontrib>Shi, Yi-Wu</creatorcontrib><creatorcontrib>Liu, Xiao-Rong</creatorcontrib><creatorcontrib>Yu, Mei-Juan</creatorcontrib><creatorcontrib>Yi, Yong-Hong</creatorcontrib><creatorcontrib>Liao, Wei-Ping</creatorcontrib><creatorcontrib>Long, Yue-Sheng</creatorcontrib><title>Promoter Analysis of Mouse Scn3a Gene and Regulation of the Promoter Activity by GC Box and CpG Methylation</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Voltage-gated sodium channel α-subunit type III (Na
v
1.3) is mainly expressed in the central nervous system and is associated with neurological disorders. The expression of mouse
Scn3a
product (Na
v
1.3) mainly occurs in embryonic and early postnatal brain but not in adult brain. Here, we report for the first time the identification and characterization of the mouse
Scn3a
gene promoter region and regulation of the promoter activity by GC box and CpG methylation. Luciferase assay showed that the promoter region F1.2 (nt −1,049 to +157) had significantly higher activity in PC12 cells, comparing with that in SH-SY5Y cells and HEK293 cells. A stepwise 5′ truncation of the promoter region found that the minimal functional promoter located within the region nt −168 to +157. Deletion of a GC box (nt −254 to −258) in the mouse
Scn3a
promoter decreased the promoter activity. CpG methylation of the F1.2 without the GC box completely repressed the promoter activity, suggesting that the GC box is a critical element in the CpG-methylated
Scn3a
promoter. These results suggest that the GC box and CpG methylation might play important roles in regulating mouse
Scn3a
gene expression.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cloning</subject><subject>CpG Islands</subject><subject>Dinucleoside Phosphates - metabolism</subject><subject>DNA Methylation</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Mice</subject><subject>Mutagenesis, Site-Directed</subject><subject>NAV1.3 Voltage-Gated Sodium Channel</subject><subject>Nervous system</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proteomics</subject><subject>Sodium</subject><subject>Sodium Channels - genetics</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</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>eNp1kEFP2zAYhq2JaS2MH7DLZHEP-z4nTuxjqUZBogKxcbbc5HMJa-NiJxP590uXbj1x8sHP81p-GPuCcIkAxbeIAlJMADHRmRaJ-sCmKKVOEPP8hE1BaZmoXOcTdhrjC4DADNUnNhEoCkwBpuzXQ_Bb31Lgs8Zu-lhH7h1f-i4S_1E2qeULaojbpuKPtO42tq19s0faZ-JHt2zr33Xb81XPF3N-5d_-GvPdgi-pfe5H7TP76Owm0vnhPGNP199_zm-Su_vF7Xx2l5RpAW1SyVLbXIEF6QoLRZVJRUJlFWCuXJWJVepyW1CRgiqk1pLAWVFiJciRq3R6xi7G3V3wrx3F1rz4Lgzfi0blGahUohogHKEy-BgDObML9daG3iCYfV0z1jVDXbOva_bO18Nwt9pS9d_4l3MAxAjE4apZUzi-_P7qH39ohBE</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Deng, Guang-Fei</creator><creator>Qin, Jia-Ming</creator><creator>Sun, Xun-Sha</creator><creator>Kuang, Zu-Ying</creator><creator>Su, Tao</creator><creator>Zhao, Qi-Hua</creator><creator>Shi, Yi-Wu</creator><creator>Liu, Xiao-Rong</creator><creator>Yu, Mei-Juan</creator><creator>Yi, Yong-Hong</creator><creator>Liao, Wei-Ping</creator><creator>Long, Yue-Sheng</creator><general>Humana Press Inc</general><general>Springer Nature 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>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20110601</creationdate><title>Promoter Analysis of Mouse Scn3a Gene and Regulation of the Promoter Activity by GC Box and CpG Methylation</title><author>Deng, Guang-Fei ; Qin, Jia-Ming ; Sun, Xun-Sha ; Kuang, Zu-Ying ; Su, Tao ; Zhao, Qi-Hua ; Shi, Yi-Wu ; Liu, Xiao-Rong ; Yu, Mei-Juan ; Yi, Yong-Hong ; Liao, Wei-Ping ; Long, Yue-Sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-d5c9a680a05f7a07d458e284d0168fd42b3f6a7e730875995e0fa2c1d2efefd93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cloning</topic><topic>CpG Islands</topic><topic>Dinucleoside Phosphates - metabolism</topic><topic>DNA Methylation</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Mice</topic><topic>Mutagenesis, Site-Directed</topic><topic>NAV1.3 Voltage-Gated Sodium Channel</topic><topic>Nervous system</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proteomics</topic><topic>Sodium</topic><topic>Sodium Channels - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deng, Guang-Fei</creatorcontrib><creatorcontrib>Qin, Jia-Ming</creatorcontrib><creatorcontrib>Sun, Xun-Sha</creatorcontrib><creatorcontrib>Kuang, Zu-Ying</creatorcontrib><creatorcontrib>Su, Tao</creatorcontrib><creatorcontrib>Zhao, Qi-Hua</creatorcontrib><creatorcontrib>Shi, Yi-Wu</creatorcontrib><creatorcontrib>Liu, Xiao-Rong</creatorcontrib><creatorcontrib>Yu, Mei-Juan</creatorcontrib><creatorcontrib>Yi, Yong-Hong</creatorcontrib><creatorcontrib>Liao, Wei-Ping</creatorcontrib><creatorcontrib>Long, Yue-Sheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deng, Guang-Fei</au><au>Qin, Jia-Ming</au><au>Sun, Xun-Sha</au><au>Kuang, Zu-Ying</au><au>Su, Tao</au><au>Zhao, Qi-Hua</au><au>Shi, Yi-Wu</au><au>Liu, Xiao-Rong</au><au>Yu, Mei-Juan</au><au>Yi, Yong-Hong</au><au>Liao, Wei-Ping</au><au>Long, Yue-Sheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Promoter Analysis of Mouse Scn3a Gene and Regulation of the Promoter Activity by GC Box and CpG Methylation</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>44</volume><issue>2</issue><spage>115</spage><epage>121</epage><pages>115-121</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>Voltage-gated sodium channel α-subunit type III (Na
v
1.3) is mainly expressed in the central nervous system and is associated with neurological disorders. The expression of mouse
Scn3a
product (Na
v
1.3) mainly occurs in embryonic and early postnatal brain but not in adult brain. Here, we report for the first time the identification and characterization of the mouse
Scn3a
gene promoter region and regulation of the promoter activity by GC box and CpG methylation. Luciferase assay showed that the promoter region F1.2 (nt −1,049 to +157) had significantly higher activity in PC12 cells, comparing with that in SH-SY5Y cells and HEK293 cells. A stepwise 5′ truncation of the promoter region found that the minimal functional promoter located within the region nt −168 to +157. Deletion of a GC box (nt −254 to −258) in the mouse
Scn3a
promoter decreased the promoter activity. CpG methylation of the F1.2 without the GC box completely repressed the promoter activity, suggesting that the GC box is a critical element in the CpG-methylated
Scn3a
promoter. These results suggest that the GC box and CpG methylation might play important roles in regulating mouse
Scn3a
gene expression.</abstract><cop>New York</cop><pub>Humana Press Inc</pub><pmid>21271300</pmid><doi>10.1007/s12031-011-9492-8</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of molecular neuroscience, 2011-06, Vol.44 (2), p.115-121 |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Cell Biology Cell Line, Tumor Cloning CpG Islands Dinucleoside Phosphates - metabolism DNA Methylation Gene expression Gene Expression Regulation Humans Mice Mutagenesis, Site-Directed NAV1.3 Voltage-Gated Sodium Channel Nervous system Neurochemistry Neurology Neurosciences Promoter Regions, Genetic - genetics Proteomics Sodium Sodium Channels - genetics |
| title | Promoter Analysis of Mouse Scn3a Gene and Regulation of the Promoter Activity by GC Box and CpG Methylation |
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