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oai:repisalud.isciii.es:20.500.12105/64972025-04-01T12:14:18Zcom_20.500.12105_2052com_20.500.12105_2051com_20.500.12105_19604col_20.500.12105_19609col_20.500.12105_19605
Repisalud author Alvaro-Blanco, Josué author Urso, Katia author Chiodo, Yuri author Martin-Cortazar, Carla author Kourani, Omar author Gomez-del Arco, Pablo author Rodriguez-Martinez, Maria author Calonge, Esther author Alcamí, José author Redondo, Juan Miguel author Iglesias, Teresa author Campanero, Miguel R funder Ministerio de Economía, Industria y Competitividad (España) funder Instituto de Salud Carlos III funder Centro de Investigación Biomedica en Red - CIBER funder Red de Investigación Cooperativa en Investigación en Sida (España) funder Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 2018-10-19T08:00:43Z 2018-10-19T08:00:43Z 2017 Nucleic Acids Res. 2017; 45(17):9960-9975 10.1093/nar/gkx641 1362-4962 0305-1048 Nucleic Acids Research 28973440 http://hdl.handle.net/20.500.12105/6497 Most E2F-binding sites repress transcription through the recruitment of Retinoblastoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Mybsp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression. eng ZINC-FINGER PROTEIN CELL-CYCLE CONTROL C-MYB TRANSCRIPTION FACTORS BINDING-SITES NEGATIVE REGULATION SIGNALING PATHWAY GENE-EXPRESSION SPLICE VARIANT RECEPTOR GENE MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter research article URL https://repisalud.isciii.es/bitstreams/55987c5c-66b5-4d69-9bcd-7f07bc0b01f2/download File MD5 4df9937eadd87b37a8eec9b97dc53e2b 5526446 application/pdf MAZInducesMYBExpression_2017.pdf URL https://repisalud.isciii.es/bitstreams/b5481c1c-0730-4810-9770-e5725884f89e/download File MD5 f6fd4a54e6fd36f969c0a43a850e8218 823912 application/pdf MAZInducesMYBExpression_2017_SUPPL.pdf URL https://repisalud.isciii.es/bitstreams/2bde78d4-cb5c-4793-9c65-5000fa089204/download File MD5 8dd95a1505cdaa3ff3524137629fa3b8 81708 text/plain MAZInducesMYBExpression_2017.pdf.txt URL https://repisalud.isciii.es/bitstreams/e80a3ef6-8f3b-4f88-b384-d10123a70bb5/download File MD5 f876c13782b8c9886fbeea3a706175b9 3426 text/plain MAZInducesMYBExpression_2017_SUPPL.pdf.txt