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FOS — RARS

Text-mined interactions from Literome

Shiohara et al., Blood 1999 (Leukemia, Myeloid) : SR11302 ( Retinoid A ), with reported anti-AP-1 activity and no activation of RARs and RXR and SR11363 ( Retinoid B ), which selectively activated RARbeta and gamma, were inactive
Dawson et al., Int J Cancer 2001 (Neoplasms, Experimental...) : Evaluation of retinoic acid receptor ( RAR ) subtype-selective alpha and gamma agonists and antagonists and a retinoid X receptor ( RXR ) class-selective agonist for efficacy at inhibiting both induction of ornithine decarboxylase (ODC) by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate ( TPA ) in mouse epidermis and rat tracheal epithelial cells and the appearance of papillomas in mouse epidermis treated in the 2-stage tumor initiation-promotion model indicated that ( i ) RXR class-selective transcriptional agonists, such as MM11246, were not involved in ODC inhibition ; ( ii ) RAR-selective agonists that induce gene transcription from RA-responsive elements ( RAREs ) were active at low concentrations ; ( iii ) RAR-selective antagonists that bind RARs and inhibit AP-1 activation on the collagenase promoter but do not activate RAREs to induce gene transcription were less effective inhibitors ; and ( iv ) RARgamma-selective retinoid agonists were more effective inhibitors of TPA induced ODC activity than RARalpha-selective agonists
Zhou et al., Mol Endocrinol 1999 : Previous in vitro results have suggested that RARs can block AP-1 DNA binding ... Our data argue for a novel mechanism by which RARs can repress AP-1 DNA binding, in which liganded RARs are able to interfere with c-Jun/c-Jun homodimerization and c-Jun/c-Fos heterodimerization and, in this way, may prevent the formation of AP-1 complexes capable of DNA binding