A Database of Drosophila Genes & Genomes

FB2012_01, released January 20th, 2012
 

Reference Report

Reference
Citation Gritzan, U., Weiss, C., Brennecke, J., Bohmann, D. (2002). Transrepression of AP-1 by nuclear receptors in Drosophila.  Mech. Dev. 115(1-2): 91--100. (Export to RIS)
FlyBase ID FBrf0149096
Publication Type Research paper
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PubMed ID 12049770
PubMed Abstract Mammalian cell culture studies have shown that several members of the nuclear receptor super family such as glucocorticoid receptor, retinoic acid receptor and thyroid hormone receptor can repress the activity of AP-1 proteins by a mechanism that does not require the nuclear receptor to bind to DNA directly, but that is otherwise poorly understood. Several aspects of nuclear receptor function are believed to rely on this inhibitory mechanism, which is referred to as transrepression. This study presents evidence that nuclear receptor-mediated transrepression of AP-1 occurs in Drosophila melanogaster. In two different developmental situations, embryonic dorsal closure and wing development, several nuclear receptors, including Seven up, Tailless, and Eagle antagonize AP-1. The inhibitory interactions with nuclear receptors are integrated with other modes of AP-1 regulation, such as mitogen-activated protein kinase signaling. A potential role of nuclear receptors in setting a threshold of AP-1 activity required for the manifestation of a cellular response is discussed.
BIOSIS ID 2002.405882
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Language of Publication English
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Publication Type Journal
Abbreviation Mech. Dev.
Title Mechanisms of Development
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Publication Year 1990-
ISBN/ISSN 0925-4773
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