Characterization of the short isoform of Helios overexpressed in patients with T‐cell malignancies
In an earlier report, we demonstrated overexpression of a short isoform of Helios, Hel‐5, which lacks three of four N‐terminal zinc fingers, in patients with adult T‐cell leukemia/lymphoma. Here, we characterized Hel‐5 using immunoprecipitation, and gel shift and luciferase promoter assays, and foun...
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| Veröffentlicht in: | Cancer science 2007-02, Vol.98 (2), p.182-188 |
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| container_title | Cancer science |
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| creator | Tabayashi, Takayuki Ishimaru, Fumihiko Takata, Minoru Kataoka, Itaru Nakase, Koichi Kozuka, Teruhiko Tanimoto, Mitsune |
| description | In an earlier report, we demonstrated overexpression of a short isoform of Helios, Hel‐5, which lacks three of four N‐terminal zinc fingers, in patients with adult T‐cell leukemia/lymphoma. Here, we characterized Hel‐5 using immunoprecipitation, and gel shift and luciferase promoter assays, and found that Hel‐5 lacks the repressor function observed with a full‐length isoform of Helios. Moreover, Hel‐5 associates with the full‐length isoforms of the Ikaros gene family, Ikaros, Aiolos and Helios, and inhibits their DNA binding activity when present in excess, leading to dominant‐negative effects on the full‐length isoforms of the Ikaros gene family. Our results suggest a critical role for Helios in the mechanism of leukemogenesis. (Cancer Sci 2007; 98: 182–188) |
| doi_str_mv | 10.1111/j.1349-7006.2006.00372.x |
| format | Article |
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Here, we characterized Hel‐5 using immunoprecipitation, and gel shift and luciferase promoter assays, and found that Hel‐5 lacks the repressor function observed with a full‐length isoform of Helios. Moreover, Hel‐5 associates with the full‐length isoforms of the Ikaros gene family, Ikaros, Aiolos and Helios, and inhibits their DNA binding activity when present in excess, leading to dominant‐negative effects on the full‐length isoforms of the Ikaros gene family. Our results suggest a critical role for Helios in the mechanism of leukemogenesis. 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Here, we characterized Hel‐5 using immunoprecipitation, and gel shift and luciferase promoter assays, and found that Hel‐5 lacks the repressor function observed with a full‐length isoform of Helios. Moreover, Hel‐5 associates with the full‐length isoforms of the Ikaros gene family, Ikaros, Aiolos and Helios, and inhibits their DNA binding activity when present in excess, leading to dominant‐negative effects on the full‐length isoforms of the Ikaros gene family. Our results suggest a critical role for Helios in the mechanism of leukemogenesis. (Cancer Sci 2007; 98: 182–188)</description><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Dimerization</subject><subject>DNA - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Ikaros Transcription Factor - classification</subject><subject>Ikaros Transcription Factor - genetics</subject><subject>Ikaros Transcription Factor - metabolism</subject><subject>Leukemia - genetics</subject><subject>Leukemia - metabolism</subject><subject>Medical sciences</subject><subject>Original</subject><subject>Protein Binding</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkctu1DAUhi0EoqXwCsgb2GXwJbYTCQlVI6BIlVhQ1pbrOWk8SuLBJ9NOWfEIPCNPgt0ZtbACL-xj-zvXnxDK2YLn9Wa94LJuK8OYXoiyMSaNWOwekeP7j8d3tqlaJsUReYa4zpCu2_opOeJGtEYrdUxWy94l52dI4bubQ5xo7OjcA8U-ppkGjF1MY3k8gyFEpPEaEuw2CRBhRcNEN9kNphnpTZh7evHrx08Pw0BHN4SryU0-AD4nTzo3ILw4nCfk64f3F8uz6vzzx0_L0_PKK2VEBY5Dl9vTTgjVaMOZdrLh_BK40Y3wtQcvfdeplSm31oGrjdLGe9XW3jTyhLzbx91sL0dY-VxWcoPdpDC6dGujC_bvnyn09ipe25w0h5A8R3h9iJDity3gbMeApR83Qdyi1S1jXEr9T1CwhikmZQabPehTREzQ3ZfDWcnL7doWzWzRzBYx7Z2YdpddX_7ZzoPjQb0MvDoADr0bulTGjQ9co1ieq8jc2z13Ewa4_e8C7PL0Szbkb3GavTw</recordid><startdate>200702</startdate><enddate>200702</enddate><creator>Tabayashi, Takayuki</creator><creator>Ishimaru, Fumihiko</creator><creator>Takata, Minoru</creator><creator>Kataoka, Itaru</creator><creator>Nakase, Koichi</creator><creator>Kozuka, Teruhiko</creator><creator>Tanimoto, Mitsune</creator><general>Blackwell Publishing Asia</general><general>Blackwell</general><scope>IQODW</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>7T5</scope><scope>7TM</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200702</creationdate><title>Characterization of the short isoform of Helios overexpressed in patients with T‐cell malignancies</title><author>Tabayashi, Takayuki ; 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Here, we characterized Hel‐5 using immunoprecipitation, and gel shift and luciferase promoter assays, and found that Hel‐5 lacks the repressor function observed with a full‐length isoform of Helios. Moreover, Hel‐5 associates with the full‐length isoforms of the Ikaros gene family, Ikaros, Aiolos and Helios, and inhibits their DNA binding activity when present in excess, leading to dominant‐negative effects on the full‐length isoforms of the Ikaros gene family. Our results suggest a critical role for Helios in the mechanism of leukemogenesis. (Cancer Sci 2007; 98: 182–188)</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>17297655</pmid><doi>10.1111/j.1349-7006.2006.00372.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Cell Line Dimerization DNA - genetics DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Gene Expression Regulation, Neoplastic Humans Ikaros Transcription Factor - classification Ikaros Transcription Factor - genetics Ikaros Transcription Factor - metabolism Leukemia - genetics Leukemia - metabolism Medical sciences Original Protein Binding Protein Isoforms - genetics Protein Isoforms - metabolism Transcription Factors - genetics Transcription Factors - metabolism Tumors |
| title | Characterization of the short isoform of Helios overexpressed in patients with T‐cell malignancies |
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