EVI1 Abrogates Interferon- Response by Selectively Blocking
نویسندگان
چکیده
From the ‡Department of Pathology and Cancer Center, University of Illinois, Chicago, Illinois 60607, the §Department of Clinical Pathology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt, the ¶Robert H. Lurie Comprehensive Cancer Center and Section of Hematology-Oncology, Northwestern University Medical School, Chicago, Illinois 60611, the Department of Pharmacology, University of Illinois, Chicago, Illinois 60607 and the **Department of Pathology, University of Chicago, Chicago, Illinois 60607
منابع مشابه
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EVI1 (Ecotropic Viral Integration site I), which was originally identified as a myeloid transforming gene by means of retroviral insertional mutagenesis in mouse leukemia, encodes a nuclear DNA binding zinc finger protein. The presence of zinc fingers that are able to bind to specific sequences of DNA suggests that EVI1 is a transcriptional regulator; however, except a few, target genes of EVI1...
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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. Here we describe the identification of a retinoic acid...
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The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced trans...
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BACKGROUND The transcription factor Ecotropic Virus Integration site 1 (EVI1) regulates cellular proliferation, differentiation, and apoptosis, and its overexpression contributes to an aggressive course of disease in myeloid leukemias and other malignancies. Notwithstanding, knowledge about the target genes mediating its biological and pathological functions remains limited. We therefore aimed ...
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تاریخ انتشار 2004