{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He Z"],"funding":["the fund of Scholar Research of Kagoshima University"],"pagination":["e2108"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11680972"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["51(1)"],"pubmed_abstract":["The mitogen-activated protein kinase kinase 4 (MKK4), a member of the MAP kinase kinase family, directly phosphorylates and activates the c-Jun NH2-terminal kinases (JNK), in response to proinflammatory cytokines and cellular stresses. Regulation of the MKK4 activity is considered to be a novel approach for the prevention and treatment of inflammation. The aim of this study was to identify whether fisetin, a potential anti-inflammatory compound, targets MKK4-JNK cascade to inhibit lipopolysaccharide (LPS)-stimulated inflammatory response. RAW264 macrophage pretreated with fisetin following LPS stimulation was used as a cell model to investigate the transactivation and expression of related-inflammatory genes by transient transfection assay, electrophoretic mobility shift assay (EMSA), or e"],"journal":["BioFactors (Oxford, England)"],"pubmed_title":["Fisetin is a selective adenosine triphosphate-competitive inhibitor for mitogen-activated protein kinase kinase 4 to inhibit lipopolysaccharide-stimulated inflammation."],"pmcid":["PMC11680972"],"funding_grant_id":["70030117"],"pubmed_authors":["Uto T","Pan X","Yang Y","He Z","Kumamoto T","Xie K","Tanigawa S","Wu S","Hou DX","Sakao K","Komatsu M"],"additional_accession":[]},"is_claimable":false,"name":"Fisetin is a selective adenosine triphosphate-competitive inhibitor for mitogen-activated protein kinase kinase 4 to inhibit lipopolysaccharide-stimulated inflammation.","description":"The mitogen-activated protein kinase kinase 4 (MKK4), a member of the MAP kinase kinase family, directly phosphorylates and activates the c-Jun NH2-terminal kinases (JNK), in response to proinflammatory cytokines and cellular stresses. Regulation of the MKK4 activity is considered to be a novel approach for the prevention and treatment of inflammation. The aim of this study was to identify whether fisetin, a potential anti-inflammatory compound, targets MKK4-JNK cascade to inhibit lipopolysaccharide (LPS)-stimulated inflammatory response. RAW264 macrophage pretreated with fisetin following LPS stimulation was used as a cell model to investigate the transactivation and expression of related-inflammatory genes by transient transfection assay, electrophoretic mobility shift assay (EMSA), or e","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan-Feb","modification":"2026-04-13T03:23:09.824Z","creation":"2025-04-04T02:48:36.665Z"},"accession":"S-EPMC11680972","cross_references":{"pubmed":["39087587"],"doi":["10.1002/biof.2108"]}}