http://purl.uniprot.org/citations/26511729 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/26511729 | http://www.w3.org/2000/01/rdf-schema#comment | "Cardiac fibrosis is a complex pathological process that includes the abnormal proliferation of cardiac fibroblasts and deposition of the extracellular matrix (ECM) proteins and collagens. Methyl-CpG-binding protein 2 (MeCP2) is a multifunctional nuclear protein, and plays a key role in the fibrotic diseases. However, the potential role of MeCP2 in cardiac fibrosis remains unclear. We report that MeCP2 modulates cardiac fibrosis via down-regulation of dual-specificity phosphatase 5 (DUSP5), a nuclear phosphatase that negatively regulates prohypertrophic signaling by ERK1/2. MeCP2 is a critical participant in the epigenetic silencing of regulatory genes. Here, we found that down-regulation of DUSP5 in cardiac fibrosis is associated with MeCP2 over-expression. Treatment of cardiac fibroblasts with MeCP2-siRNA blocked proliferation. Knockdown of MeCP2 elevated DUSP5 expression in activated cardiac fibroblasts. Moreover, we investigated the effect of DUSP5 on the ERK1/2 activation. Our results demonstrated that MeCP2 modulates DUSP5 mediated activation of ERK1/2 in cardiac fibrosis. Taken together, these results indicated that MeCP2 acts as a key regulator of pathological cardiac fibrosis, promotes cardiac fibroblasts proliferation and fibrosis by down-regulation of DUSP5."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ijbiomac.2015.10.076"xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/author | "Hu W."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/author | "Yang J.J."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/author | "Tao H."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/author | "Deng Z.Y."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/author | "Shi K.H."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/name | "Int J Biol Macromol"xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/pages | "68-75"xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/title | "MeCP2 regulation of cardiac fibroblast proliferation and fibrosis by down-regulation of DUSP5."xsd:string |
http://purl.uniprot.org/citations/26511729 | http://purl.uniprot.org/core/volume | "82"xsd:string |
http://purl.uniprot.org/citations/26511729 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26511729 |
http://purl.uniprot.org/citations/26511729 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/26511729 |
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http://purl.uniprot.org/uniprot/#_A6JHW1-mappedCitation-26511729 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26511729 |
http://purl.uniprot.org/uniprot/#_O54838-mappedCitation-26511729 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26511729 |
http://purl.uniprot.org/uniprot/O54838 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/26511729 |
http://purl.uniprot.org/uniprot/A6JHW0 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/26511729 |
http://purl.uniprot.org/uniprot/A6JHW1 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/26511729 |