| http://purl.uniprot.org/citations/37642020 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/37642020 | http://www.w3.org/2000/01/rdf-schema#comment | "Background Pathological cardiac hypertrophy is a major cause of heart failure morbidity. The complex mechanism of intermolecular interactions underlying the pathogenesis of cardiac hypertrophy has led to a lack of development and application of therapeutic methods. Methods and Results Our study provides the first evidence that TRAF4, a member of the tumor necrosis factor receptor-associated factor (TRAF) family, acts as a promoter of cardiac hypertrophy. Here, Western blotting assays demonstrated that TRAF4 is upregulated in cardiac hypertrophy. Additionally, TRAF4 deletion inhibits the development of cardiac hypertrophy in a mouse model after transverse aortic constriction surgery, whereas its overexpression promotes phenylephrine stimulation-induced cardiomyocyte hypertrophy in primary neonatal rat cardiomyocytes. Mechanistically, RNA-seq analysis revealed that TRAF4 promoted the activation of the protein kinase B pathway during cardiac hypertrophy. Moreover, we found that inhibition of protein kinase B phosphorylation rescued the aggravated cardiomyocyte hypertrophic phenotypes caused by TRAF4 overexpression in phenylephrine-treated neonatal rat cardiomyocytes, suggesting that TRAF4 may regulate cardiac hypertrophy in a protein kinase B-dependent manner. Conclusions Our results revealed the regulatory function of TRAF4 in cardiac hypertrophy, which may provide new insights into developing therapeutic and preventive targets for this disease."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.org/dc/terms/identifier | "doi:10.1161/jaha.122.028185"xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Wan F."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Tu J."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Wang C.Q."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Li H.P."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Deng K.Q."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/author | "Xiao W.C."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/name | "J Am Heart Assoc"xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/pages | "e028185"xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/title | "TRAF Family Member 4 Promotes Cardiac Hypertrophy Through the Activation of the AKT Pathway."xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://purl.uniprot.org/core/volume | "12"xsd:string |
| http://purl.uniprot.org/citations/37642020 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/37642020 |
| http://purl.uniprot.org/citations/37642020 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/37642020 |
| http://purl.uniprot.org/uniprot/#_Q61382-mappedCitation-37642020 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37642020 |
| http://purl.uniprot.org/uniprot/Q61382 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/37642020 |