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Transcriptional regulation of the vimentin-encoding gene in mouse myeloid leukemia M1 cells
To investigate the regulatory mechanisms controlling expression of the vimentin-encoding gene ( Vim) during mouse myeloid leukemia M1 cell differentiation, mouse Vim was cloned and the transcriptional activity of its 5′ promoter region was analysed by chloramphenicol acetyltransferase (CAT) assay. A...
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Published in: | Gene 1995-12, Vol.166 (2), p.281-286 |
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container_title | Gene |
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creator | Nakamura, Nobuhiro Shida, Miho Hirayoshi, Kazunori Nagata, Kazuhiro |
description | To investigate the regulatory mechanisms controlling expression of the vimentin-encoding gene (
Vim) during mouse myeloid leukemia M1 cell differentiation, mouse
Vim was cloned and the transcriptional activity of its 5′ promoter region was analysed by chloramphenicol acetyltransferase (CAT) assay. Analyses of various deletion mutants revealed that a 188-bp fragment of the proximal
Vim promoter (
pVim) was sufficient for effective transcription in M1 cells. This 188-bp sequence is highly conserved between mouse, hamster and human. Further deletion analyses revealed that a minimum promoter element (−44 to + 26) is essential for basic promoter function and could respond to cell differentiation. Detailed analyses of mutant and chimeric
pVim constructs defined a CCAAT box at −89 to −84 to be an essential positive regulatory element. A G + C-rich element between the CCAAT and TATA boxes was found to act as a strong negative regulatory element in
Vim transcription. |
doi_str_mv | 10.1016/0378-1119(95)00600-1 |
format | article |
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Vim) during mouse myeloid leukemia M1 cell differentiation, mouse
Vim was cloned and the transcriptional activity of its 5′ promoter region was analysed by chloramphenicol acetyltransferase (CAT) assay. Analyses of various deletion mutants revealed that a 188-bp fragment of the proximal
Vim promoter (
pVim) was sufficient for effective transcription in M1 cells. This 188-bp sequence is highly conserved between mouse, hamster and human. Further deletion analyses revealed that a minimum promoter element (−44 to + 26) is essential for basic promoter function and could respond to cell differentiation. Detailed analyses of mutant and chimeric
pVim constructs defined a CCAAT box at −89 to −84 to be an essential positive regulatory element. A G + C-rich element between the CCAAT and TATA boxes was found to act as a strong negative regulatory element in
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Vim) during mouse myeloid leukemia M1 cell differentiation, mouse
Vim was cloned and the transcriptional activity of its 5′ promoter region was analysed by chloramphenicol acetyltransferase (CAT) assay. Analyses of various deletion mutants revealed that a 188-bp fragment of the proximal
Vim promoter (
pVim) was sufficient for effective transcription in M1 cells. This 188-bp sequence is highly conserved between mouse, hamster and human. Further deletion analyses revealed that a minimum promoter element (−44 to + 26) is essential for basic promoter function and could respond to cell differentiation. Detailed analyses of mutant and chimeric
pVim constructs defined a CCAAT box at −89 to −84 to be an essential positive regulatory element. A G + C-rich element between the CCAAT and TATA boxes was found to act as a strong negative regulatory element in
Vim transcription.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>CCAAT box</subject><subject>Cell Differentiation</subject><subject>Cloning, Molecular</subject><subject>Differentiation</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Intermediate filament</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Mice</subject><subject>Molecular Sequence Data</subject><subject>negative regulatory element</subject><subject>promoter analysis</subject><subject>Promoter Regions, Genetic</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Neoplasm - genetics</subject><subject>transfection</subject><subject>Tumor Cells, Cultured</subject><subject>Vimentin - genetics</subject><issn>0378-1119</issn><issn>1879-0038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><recordid>eNqFkE1PwzAMhiMEGuPjH4CUE4JDIW6bpr0goYkvaYjLOHGIstYdgTYZSTtp_56UTTuCL5Hj16_th5AzYNfAILthicgjACguC37FWMZYBHtkDLkoIsaSfJ-Md5JDcuT9JwvBeTwio5ynCYhsTN5nThlfOr3stDWqoQ4XfaOGhNqadh9IV7pF02kToSltpc2CLtAg1Ya2tvdI2zU2Vle0wf4LW63oC9ASm8afkINaNR5Pt-8xeXu4n02eounr4_PkbhqVKU-7CETBsyRhbF7HdSZEBnGusOLhlyseTuCVmtdclBVnHCGJFSQqhmyeKxguSo7JxcZ36ex3j76TrfbDBspg2FCK4JnyOP9XCCLwiTMRhOlGWDrrvcNaLp1ulVtLYHKALweyciArCy5_4UsIbedb_37eYrVr2tIO9dtNHQONlUYnfakDVay0w7KTldV_D_gBKeKSTQ</recordid><startdate>19951212</startdate><enddate>19951212</enddate><creator>Nakamura, Nobuhiro</creator><creator>Shida, Miho</creator><creator>Hirayoshi, Kazunori</creator><creator>Nagata, Kazuhiro</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19951212</creationdate><title>Transcriptional regulation of the vimentin-encoding gene in mouse myeloid leukemia M1 cells</title><author>Nakamura, Nobuhiro ; Shida, Miho ; Hirayoshi, Kazunori ; Nagata, Kazuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-179563300bf2f6776128aed59565a50375dabf57cd505e132a13a216b8a100003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>CCAAT box</topic><topic>Cell Differentiation</topic><topic>Cloning, Molecular</topic><topic>Differentiation</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Intermediate filament</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Mice</topic><topic>Molecular Sequence Data</topic><topic>negative regulatory element</topic><topic>promoter analysis</topic><topic>Promoter Regions, Genetic</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Neoplasm - genetics</topic><topic>transfection</topic><topic>Tumor Cells, Cultured</topic><topic>Vimentin - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakamura, Nobuhiro</creatorcontrib><creatorcontrib>Shida, Miho</creatorcontrib><creatorcontrib>Hirayoshi, Kazunori</creatorcontrib><creatorcontrib>Nagata, Kazuhiro</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Gene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakamura, Nobuhiro</au><au>Shida, Miho</au><au>Hirayoshi, Kazunori</au><au>Nagata, Kazuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcriptional regulation of the vimentin-encoding gene in mouse myeloid leukemia M1 cells</atitle><jtitle>Gene</jtitle><addtitle>Gene</addtitle><date>1995-12-12</date><risdate>1995</risdate><volume>166</volume><issue>2</issue><spage>281</spage><epage>286</epage><pages>281-286</pages><issn>0378-1119</issn><eissn>1879-0038</eissn><abstract>To investigate the regulatory mechanisms controlling expression of the vimentin-encoding gene (
Vim) during mouse myeloid leukemia M1 cell differentiation, mouse
Vim was cloned and the transcriptional activity of its 5′ promoter region was analysed by chloramphenicol acetyltransferase (CAT) assay. Analyses of various deletion mutants revealed that a 188-bp fragment of the proximal
Vim promoter (
pVim) was sufficient for effective transcription in M1 cells. This 188-bp sequence is highly conserved between mouse, hamster and human. Further deletion analyses revealed that a minimum promoter element (−44 to + 26) is essential for basic promoter function and could respond to cell differentiation. Detailed analyses of mutant and chimeric
pVim constructs defined a CCAAT box at −89 to −84 to be an essential positive regulatory element. A G + C-rich element between the CCAAT and TATA boxes was found to act as a strong negative regulatory element in
Vim transcription.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>8543176</pmid><doi>10.1016/0378-1119(95)00600-1</doi><tpages>6</tpages></addata></record> |
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ispartof | Gene, 1995-12, Vol.166 (2), p.281-286 |
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source | ScienceDirect Journals |
subjects | Animals Base Sequence CCAAT box Cell Differentiation Cloning, Molecular Differentiation Gene Expression Regulation, Developmental Gene Expression Regulation, Neoplastic Intermediate filament Leukemia, Myeloid - genetics Mice Molecular Sequence Data negative regulatory element promoter analysis Promoter Regions, Genetic RNA, Messenger - genetics RNA, Neoplasm - genetics transfection Tumor Cells, Cultured Vimentin - genetics |
title | Transcriptional regulation of the vimentin-encoding gene in mouse myeloid leukemia M1 cells |
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