TAILIEUCHUNG - Báo cáo khoa học: Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid (ATRA) and acts as a dual modulator of the ATRA response

Ecotropic viral integration site 1(EVI1) plays important roles in leukaemia and development, and its expression is temporally and spatially highly restricted during the latter process. Nevertheless, the only physiological agent that to date has been shown to regulate transcription of this gene in mammalian cells is all-trans retinoic acid. | ễFEBS Journal Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid ATRA and acts as a dual modulator of the ATRA response Sonja C. Bingemann1 Torsten A. Konrad1 and Rotraud Wieser1 2 1 Department of MedicalGenetics MedicalUniversity of Vienna Austria 2 Department of Medicine I MedicalUniversity of Vienna Austria Keywords all-trans retinoic acid EVI1 feedback inhibition RARE transcription regulation Correspondence R. Wieser Clinic of Medicine I Medical University of Vienna Waehringer Guertel 18-20 1090 Vienna Austria E-mail Re-use of this article is permitted in accordance with the Terms and Conditions set out at http . com authorresources Received 11 June 2009 revised 15 August 2009 accepted 22 September 2009 doi Ecotropic viral integration site 1 EVI plays important roles in leukaemia and development and its expression is temporally and spatially highly restricted during the latter process. Nevertheless the only physiological agent that to date has been shown to regulate transcription of this gene in mammalian cells is all-trans retinoic acid. Here we describe the identification of a retinoic acid response element that was located in the most distal of several alternative first exons of the human EVI1 gene and was constitutively bound by canonical retinoid receptors in NTERA-2 teratocarcinoma cells. Furthermore it was the target of negative feedback by EVI1 on the induction of its own promoter by retinoic acid. This process required a previously described transcription repression domain of EVI1. Extending its role as a modulator of the retinoic acid response EVI1 had the opposite effect on the RARb retinoic acid response element whose induction by all-trans retinoic acid it enhanced through a mechanism that involved almost all of its known functional domains. Augmentation of the retinoic acid response by EVI1

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