The rapamycin sensitivity of human T-cell leukaemia virus type I-induced T-cell proliferation is mediated independently of the polypyrimidine motifs in the 5' long terminal repeat
Department of Medicine, University of Cambridge, Level 5, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK 1 Author for correspondence: Nicola Rose. Fax +44 1223 336846. e-mail njr1004{at}mole.bio.cam.ac.uk The immunosuppressant rapamycin can regulate the translation of a subset of messenge...
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Veröffentlicht in: | Journal of general virology 2001-02, Vol.82 (2), p.435-439 |
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creator | Rose, Nicola J Lever, Andrew M. L |
description | Department of Medicine, University of Cambridge, Level 5, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK 1
Author for correspondence: Nicola Rose. Fax +44 1223 336846. e-mail njr1004{at}mole.bio.cam.ac.uk
The immunosuppressant rapamycin can regulate the translation of a subset of messenger RNAs, a phenotype which has been linked to the presence of a polypyrimidine motif [C(N) 414 ] downstream of the mRNA cap structure. T-cell clones naturally infected with transcriptionally active human T-cell leukaemia virus, type I (HTLV-I) undergo autologous proliferation; this phenotype is inhibited by rapamycin but not FK506, which reverses the rapamycin effect. Within the R region of the HTLV-I 5' long terminal repeat (LTR) there are seven polypyrimidine motifs. We sought to determine if these were involved in the sensitivity of proliferation to the presence of rapamycin. Here we illustrate the generation of an in vitro model of this rapamycin-sensitivity and the analysis of LTR mutants which were created to determine the importance of the polypyrimidine motifs. Reporter gene assays suggest the effect is independent of the polypyrimidine motifs in the virus leader sequence. |
doi_str_mv | 10.1099/0022-1317-82-2-435 |
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Author for correspondence: Nicola Rose. Fax +44 1223 336846. e-mail njr1004{at}mole.bio.cam.ac.uk
The immunosuppressant rapamycin can regulate the translation of a subset of messenger RNAs, a phenotype which has been linked to the presence of a polypyrimidine motif [C(N) 414 ] downstream of the mRNA cap structure. T-cell clones naturally infected with transcriptionally active human T-cell leukaemia virus, type I (HTLV-I) undergo autologous proliferation; this phenotype is inhibited by rapamycin but not FK506, which reverses the rapamycin effect. Within the R region of the HTLV-I 5' long terminal repeat (LTR) there are seven polypyrimidine motifs. We sought to determine if these were involved in the sensitivity of proliferation to the presence of rapamycin. Here we illustrate the generation of an in vitro model of this rapamycin-sensitivity and the analysis of LTR mutants which were created to determine the importance of the polypyrimidine motifs. Reporter gene assays suggest the effect is independent of the polypyrimidine motifs in the virus leader sequence.</description><identifier>ISSN: 0022-1317</identifier><identifier>EISSN: 1465-2099</identifier><identifier>DOI: 10.1099/0022-1317-82-2-435</identifier><identifier>PMID: 11161283</identifier><language>eng</language><publisher>England: Soc General Microbiol</publisher><subject>Animals ; Base Sequence ; Cell Division - drug effects ; COS Cells ; Gene Expression Regulation - drug effects ; Gene Products, rex - genetics ; Gene Products, rex - metabolism ; Gene Products, tax - genetics ; Gene Products, tax - metabolism ; Genes, Reporter - genetics ; human T-lymphotropic virus 1 ; Human T-lymphotropic virus 1 - drug effects ; Human T-lymphotropic virus 1 - genetics ; Human T-lymphotropic virus 1 - physiology ; Humans ; Immunosuppressive Agents - pharmacology ; Jurkat Cells ; Models, Biological ; Mutation - genetics ; polypyrimidines ; rapamycin ; Sirolimus - antagonists & inhibitors ; Sirolimus - pharmacology ; T-Lymphocytes - cytology ; T-Lymphocytes - drug effects ; Tacrolimus - pharmacology ; Terminal Repeat Sequences - genetics ; Transfection</subject><ispartof>Journal of general virology, 2001-02, Vol.82 (2), p.435-439</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-1d86590271669f8e6bd7b7fe842ac97267a15a00972bef47f08b166cefa725e03</citedby><cites>FETCH-LOGICAL-c406t-1d86590271669f8e6bd7b7fe842ac97267a15a00972bef47f08b166cefa725e03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3746,3747,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11161283$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rose, Nicola J</creatorcontrib><creatorcontrib>Lever, Andrew M. L</creatorcontrib><title>The rapamycin sensitivity of human T-cell leukaemia virus type I-induced T-cell proliferation is mediated independently of the polypyrimidine motifs in the 5' long terminal repeat</title><title>Journal of general virology</title><addtitle>J Gen Virol</addtitle><description>Department of Medicine, University of Cambridge, Level 5, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK 1
Author for correspondence: Nicola Rose. Fax +44 1223 336846. e-mail njr1004{at}mole.bio.cam.ac.uk
The immunosuppressant rapamycin can regulate the translation of a subset of messenger RNAs, a phenotype which has been linked to the presence of a polypyrimidine motif [C(N) 414 ] downstream of the mRNA cap structure. T-cell clones naturally infected with transcriptionally active human T-cell leukaemia virus, type I (HTLV-I) undergo autologous proliferation; this phenotype is inhibited by rapamycin but not FK506, which reverses the rapamycin effect. Within the R region of the HTLV-I 5' long terminal repeat (LTR) there are seven polypyrimidine motifs. We sought to determine if these were involved in the sensitivity of proliferation to the presence of rapamycin. Here we illustrate the generation of an in vitro model of this rapamycin-sensitivity and the analysis of LTR mutants which were created to determine the importance of the polypyrimidine motifs. Reporter gene assays suggest the effect is independent of the polypyrimidine motifs in the virus leader sequence.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Cell Division - drug effects</subject><subject>COS Cells</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Products, rex - genetics</subject><subject>Gene Products, rex - metabolism</subject><subject>Gene Products, tax - genetics</subject><subject>Gene Products, tax - metabolism</subject><subject>Genes, Reporter - genetics</subject><subject>human T-lymphotropic virus 1</subject><subject>Human T-lymphotropic virus 1 - drug effects</subject><subject>Human T-lymphotropic virus 1 - genetics</subject><subject>Human T-lymphotropic virus 1 - physiology</subject><subject>Humans</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Jurkat Cells</subject><subject>Models, Biological</subject><subject>Mutation - genetics</subject><subject>polypyrimidines</subject><subject>rapamycin</subject><subject>Sirolimus - antagonists & inhibitors</subject><subject>Sirolimus - pharmacology</subject><subject>T-Lymphocytes - cytology</subject><subject>T-Lymphocytes - drug effects</subject><subject>Tacrolimus - pharmacology</subject><subject>Terminal Repeat Sequences - genetics</subject><subject>Transfection</subject><issn>0022-1317</issn><issn>1465-2099</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi1ERbeFF-CAfKInU9tJ7OSIKqCVKvWyPVtOMt4dSJxgO0V5Ll4Qb3cpRy62pfnmH40_Qt4L_knwprnmXEomCqFZLZlkZVG9IhtRqorJXH5NNi_AObmI8Tvnoiwr_YacCyGUkHWxIb-3e6DBznZcO_Q0go-Y8AnTSidH98toPd2yDoaBDrD8sDCipU8YlkjTOgO9Y-j7pYP-LzWHaUAHwSacPMVIR-jRpgxkEGbIh0_Dc3rKo-dpWOc14Ig9eqDjlNDFjD4Xqys6TH5HE4QRvR1oyAE2vSVnzg4R3p3uS_L49cv25pbdP3y7u_l8z7qSq8REX6uq4VILpRpXg2p73WoHdSlt12iptBWV5Tw_W3CldrxuM9qBs1pWwItL8vGYm3f6uUBMZsR4WNJ6mJZoNFdFJWv5X1BoXTZFrTMoj2AXphgDODPn1W1YjeDm4NQclJmDMlNLI012mps-nNKXNn_mv5aTxAxcHYE97va_MIDZgR8xz2hxMlnWS9QfVlytrA</recordid><startdate>20010201</startdate><enddate>20010201</enddate><creator>Rose, Nicola J</creator><creator>Lever, Andrew M. L</creator><general>Soc General Microbiol</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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20010201</creationdate><title>The rapamycin sensitivity of human T-cell leukaemia virus type I-induced T-cell proliferation is mediated independently of the polypyrimidine motifs in the 5' long terminal repeat</title><author>Rose, Nicola J ; Lever, Andrew M. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-1d86590271669f8e6bd7b7fe842ac97267a15a00972bef47f08b166cefa725e03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Cell Division - drug effects</topic><topic>COS Cells</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Products, rex - genetics</topic><topic>Gene Products, rex - metabolism</topic><topic>Gene Products, tax - genetics</topic><topic>Gene Products, tax - metabolism</topic><topic>Genes, Reporter - genetics</topic><topic>human T-lymphotropic virus 1</topic><topic>Human T-lymphotropic virus 1 - drug effects</topic><topic>Human T-lymphotropic virus 1 - genetics</topic><topic>Human T-lymphotropic virus 1 - physiology</topic><topic>Humans</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Jurkat Cells</topic><topic>Models, Biological</topic><topic>Mutation - genetics</topic><topic>polypyrimidines</topic><topic>rapamycin</topic><topic>Sirolimus - antagonists & inhibitors</topic><topic>Sirolimus - pharmacology</topic><topic>T-Lymphocytes - cytology</topic><topic>T-Lymphocytes - drug effects</topic><topic>Tacrolimus - pharmacology</topic><topic>Terminal Repeat Sequences - genetics</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rose, Nicola J</creatorcontrib><creatorcontrib>Lever, Andrew M. 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L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The rapamycin sensitivity of human T-cell leukaemia virus type I-induced T-cell proliferation is mediated independently of the polypyrimidine motifs in the 5' long terminal repeat</atitle><jtitle>Journal of general virology</jtitle><addtitle>J Gen Virol</addtitle><date>2001-02-01</date><risdate>2001</risdate><volume>82</volume><issue>2</issue><spage>435</spage><epage>439</epage><pages>435-439</pages><issn>0022-1317</issn><eissn>1465-2099</eissn><abstract>Department of Medicine, University of Cambridge, Level 5, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK 1
Author for correspondence: Nicola Rose. Fax +44 1223 336846. e-mail njr1004{at}mole.bio.cam.ac.uk
The immunosuppressant rapamycin can regulate the translation of a subset of messenger RNAs, a phenotype which has been linked to the presence of a polypyrimidine motif [C(N) 414 ] downstream of the mRNA cap structure. T-cell clones naturally infected with transcriptionally active human T-cell leukaemia virus, type I (HTLV-I) undergo autologous proliferation; this phenotype is inhibited by rapamycin but not FK506, which reverses the rapamycin effect. Within the R region of the HTLV-I 5' long terminal repeat (LTR) there are seven polypyrimidine motifs. We sought to determine if these were involved in the sensitivity of proliferation to the presence of rapamycin. Here we illustrate the generation of an in vitro model of this rapamycin-sensitivity and the analysis of LTR mutants which were created to determine the importance of the polypyrimidine motifs. Reporter gene assays suggest the effect is independent of the polypyrimidine motifs in the virus leader sequence.</abstract><cop>England</cop><pub>Soc General Microbiol</pub><pmid>11161283</pmid><doi>10.1099/0022-1317-82-2-435</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Base Sequence Cell Division - drug effects COS Cells Gene Expression Regulation - drug effects Gene Products, rex - genetics Gene Products, rex - metabolism Gene Products, tax - genetics Gene Products, tax - metabolism Genes, Reporter - genetics human T-lymphotropic virus 1 Human T-lymphotropic virus 1 - drug effects Human T-lymphotropic virus 1 - genetics Human T-lymphotropic virus 1 - physiology Humans Immunosuppressive Agents - pharmacology Jurkat Cells Models, Biological Mutation - genetics polypyrimidines rapamycin Sirolimus - antagonists & inhibitors Sirolimus - pharmacology T-Lymphocytes - cytology T-Lymphocytes - drug effects Tacrolimus - pharmacology Terminal Repeat Sequences - genetics Transfection |
title | The rapamycin sensitivity of human T-cell leukaemia virus type I-induced T-cell proliferation is mediated independently of the polypyrimidine motifs in the 5' long terminal repeat |
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