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pubmed-article:21571370pubmed:abstractTextInterleukin 1? (IL-1?) is a pro-inflammatory cytokine secreted by activated macrophages and monocytes. Previously, we have reported that bone morphogenetic protein-6 (BMP-6) induces inducible nitric oxide synthase (iNOS) expression via IL-1? in macrophages. In the present study, we demonstrate that BMP-6 increases IL-1? expression in macrophages via the receptors ALK3 and BMPRII as well as the downstream signaling protein Smad1. Surprisingly though, inhibition of the ERK and JNK non-Smad pathways also completely blocked the induction of IL-1? by BMP-6 in macrophages. Further analysis revealed that a physical interaction between the transcription factor PU.1 and Smad 1 is necessary for the upregulation of IL-1? expression by BMP-6 in macrophages. Taken together, these results demonstrate that BMP-6-induced IL-1? expression in macrophages is mediated via a cross-talk between the Smad and the non-Smad pathways through Smad1 and PU.1.lld:pubmed
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pubmed-article:21571370pubmed:authorpubmed-author:LeeJae-HoJHlld:pubmed
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pubmed-article:21571370pubmed:copyrightInfoCopyright © 2011 Elsevier Ltd. All rights reserved.lld:pubmed
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pubmed-article:21571370pubmed:articleTitleBone morphogenetic protein 6-induced interleukin-1? expression in macrophages requires PU.1/Smad1 interaction.lld:pubmed
pubmed-article:21571370pubmed:affiliationSection of Urologic Oncology and the Dean and Betty Gallo Prostate Cancer Center, The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, 195 Little Albany Street #4560, New Brunswick, NJ 08903, United States.lld:pubmed
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