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New insights into TGF-beta-Smad signalling 总被引:1,自引:0,他引:1
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TGF-beta signalling through the Smad pathway 总被引:2,自引:0,他引:2
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A Nakao T Imamura S Souchelnytskyi M Kawabata A Ishisaki E Oeda K Tamaki J Hanai C H Heldin K Miyazono P ten Dijke 《The EMBO journal》1997,16(17):5353-5362
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How the Smads regulate transcription 总被引:4,自引:0,他引:4
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The Smads 总被引:8,自引:0,他引:8
Hill CS 《The international journal of biochemistry & cell biology》1999,31(11):1249-1254
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TLR agonists regulate PDGF-B production and cell proliferation through TGF-beta/type I IFN crosstalk
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Transforming growth factor-beta (TGF-beta) and type I interferon (IFN) autocrine/paracrine loops are recognized as key mediators of signaling cascades that control a variety of cellular functions. Here, we describe a novel mechanism by which Toll-like receptor (TLR) agonists utilize these two autocrine/paracrine loops to differentially regulate the induction of PDGF-B, a growth factor implicated in a number of diseases ranging from tumor metastasis to glomerulonephritis. We demonstrate that CpG-specific induction of PDGF-B requires activation of Smads through TGFbeta1 autocrine/paracrine signaling. In contrast, polyinosinic:polycytidylic acid strongly represses CpG's as well as its own intrinsic ability to induce PDGF-B mRNA through type I IFN-mediated induction of Smad7, a negative regulator of Smad3/4. Furthermore, we have shown that this crosstalk mechanism translates into similar regulation of mesangial cell proliferation. Thus, our results demonstrate the importance of crosstalk between TGF-beta and type I IFNs in determining the specificity of TLR-mediated gene induction. 相似文献
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Regulation of cell proliferation by Smad proteins 总被引:40,自引:0,他引:40