Fig. 6

Target identification And molecular interactions of ENL And 1-OHPHE in endometriosis. (A) KEGG enrichment analysis of biological processes for ENL targets in endometriosis. (B) GO pathway analysis of ENL targets in endometriosis. (C) KEGG enrichment Analysis of biological processes for 1-OHPHE targets in endometriosis. (D) GO pathway Analysis of 1-OHPHE targets in endometriosis. (E) Intersection of KEGG and GO enrichment results for ESR1 and GRB2. (F-G) Molecular docking analysis of ENL binding to ESR1 and XDH complexes. (H) Molecular docking Analysis of 1-OHPHE binding to GRB2 complexes. (I) RMSD from molecular dynamics simulations of XDH and ENL. (J) RMSF from molecular dynamics simulations of XDH with ENL. The red boxes highlight the pathways among the top 20 enriched pathways that involve ESR1 and GRB2, while the green squares indicate the pathways that are shared by both. (K) Overview of XDH catalytic mechanism in oxidizing hypoxanthine to xanthine, and xanthine to UA via Moco, [2Fe-2 S], and FAD. ENL blocks the electron transfer of Moco, [2Fe-2 S], and FAD in the enzymatic process by binding to the FAD site. RMSD root mean square deviation RMSF root mean square fluctuation ENL enterolactone UA uric acid FAD Flavin adenine dinucleotide Moco Molybdenum Cofactor.