| http://purl.uniprot.org/citations/26129946 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26129946 | http://www.w3.org/2000/01/rdf-schema#comment | "Glycogen synthase kinase (GSK)-3β, a serine/threonine kinase with an inhibitory role in glycogen synthesis in hepatocytes and skeletal muscle, is also expressed in cardiac and smooth muscles. Inhibition of GSK-3β results in cardiac hypertrophy through reducing phosphorylation and increasing transcriptional activity of myocardin, a transcriptional co-activator for serum response factor. Myocardin plays critical roles in differentiation of smooth muscle cells (SMCs). This study, therefore, aimed to examine whether and how inhibition of GSK-3β regulates myocardin activity in human vascular SMCs. Treatment of SMCs with the GSK-3β inhibitors AR-A014418 and TWS 119 significantly reduced endogenous myocardin activity, as indicated by lower expression of myocardin target genes (and gene products), CNN1 (calponin), TAGLN1 (SM22), and ACTA2 (SM α-actin). In human SMCs overexpressing myocardin through the T-REx system, treatment with either GSK-3β inhibitor also inhibited the expression of CNN1, TAGLN1, and ACTA2. These effects of GSK-3β inhibitors were mimicked by transfection with GSK-3β siRNA. Notably, both AR-A014418 and TWS 119 decreased the serine/threonine phosphorylation of myocardin. The chromatin immunoprecipitation assay showed that AR-A014418 treatment reduced myocardin occupancy of the promoter of the myocardin target gene ACTA2. Overexpression of a dominant-negative GSK-3β mutant in myocardin-overexpressing SMCs reduced the expression of calponin, SM22, and SM α-actin. As expected, overexpression of constitutively active or wild-type GSK-3β in SMCs without myocardin overexpression increased expression of these proteins. In summary, our results indicate that inhibition of GSK-3β reduces myocardin transcriptional activity, suggesting a role for GSK-3β in myocardin transcriptional activity and smooth muscle differentiation."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.25084"xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Li L."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Shi Z."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Yin H."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Singh P."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Gui Y."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Zheng X.L."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Walsh M.P."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Zhou Y.X."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/author | "Yu Y.N."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/pages | "393-402"xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/title | "Potential Role of Glycogen Synthase Kinase-3beta in Regulation of Myocardin Activity in Human Vascular Smooth Muscle Cells."xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://purl.uniprot.org/core/volume | "231"xsd:string |
| http://purl.uniprot.org/citations/26129946 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26129946 |
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