http://purl.uniprot.org/citations/25245272 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25245272 | http://www.w3.org/2000/01/rdf-schema#comment | "Tissue inhibitor of metalloproteinase-3 (TIMP-3) is an important natural inhibitor of matrix metalloproteinases (MMPs) and of a disintegrin and metalloproteinase with thrombospondin motif (ADAMTs), which can cleave cartilage extracellular matrix components to cause cartilage degradation. In this study, our data suggest TGF-β1 induces TIMP-3 expression through activations of both the ERK1/2 and Smad2/3 signaling pathways. TGF-β1-stimulated TIMP-3 expression was significantly inhibited by SB525334 (TGF-β receptor I kinase inhibitor), accompanied by a reduction in ERK1/2 and Smad3 phosphorylation. We used PD98059 (MEK inhibitor) and SIS3 (inhibitor of Smad3 phosphorylation) to investigate the respective roles of ERK1/2 and Smad2/3 signaling pathways in TGF-β1-induced TIMP-3 expression. The results show PD98059 treatment significantly suppressed TGF-β1-induced ERK1/2 phosphorylation and TIMP-3 expression. Under these conditions, the degree of Smad3 phosphorylation correlated with ERK1/2 activation, which suggests that ERK1/2 may activate Smad3 phosphorylation. SIS3 significantly inhibited TGF-β1-induced Smad3 phosphorylation and TIMP-3 expression. ERK1/2 phosphorylation alone had no effect on TGF-β1-induced TIMP-3 expression, which suggests ERK1/2 via Smad3 phosphorylation regulates TGF-β1-induced TIMP-3 expression. Here, we demonstrate that ERK1/2 may be capable of activating the Smad2/3 signaling pathway to result in TGF-β1-induced TIMP-3 up-regulation."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.abb.2014.09.009"xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Fan C."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Hu X."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Lu X."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Zhu Y."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Jin C."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/author | "Tao H."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/name | "Arch Biochem Biophys"xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/pages | "229-236"xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/title | "Interaction of ERK1/2 and Smad2/3 signaling pathways in TGF-beta1-induced TIMP-3 expression in rat chondrocytes."xsd:string |
http://purl.uniprot.org/citations/25245272 | http://purl.uniprot.org/core/volume | "564"xsd:string |
http://purl.uniprot.org/citations/25245272 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25245272 |
http://purl.uniprot.org/citations/25245272 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25245272 |
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http://purl.uniprot.org/uniprot/#_A6KMS9-mappedCitation-25245272 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/25245272 |
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http://purl.uniprot.org/uniprot/#_F7FFD0-mappedCitation-25245272 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/25245272 |