Ask about this productRelated genes to: IL1b protein
- Gene:
- IL1B NIH gene
- Name:
- interleukin 1 beta
- Previous symbol:
- -
- Synonyms:
- IL1F2, IL-1B, IL1-BETA
- Chromosome:
- 2q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-31
- Date modifiied:
- 2016-10-05
Related products to: IL1b protein
Related articles to: IL1b protein
- This study was conducted to delineate layer-specific transcriptomic alterations in the keratoconus (KC) epithelium and stroma and to identify potential biomarkers using machine learning (ML)-based analysis. - Source: PubMed
Publication date: 2026/05/08
Du KaiyuePeng RongmeiXiao GegeQu YiHan LiangHong Jing - Inflammatory cytokines, particularly interleukin-1β (IL-1β), have a main role in diabetic nephropathy (DN) pathogenesis. Genetic variations within the IL1B promoter region may modulate cytokine expression and affect vulnerability to renal injury in type 2 diabetes mellitus (T2DM). We aimed to assess the correlation between the IL1B (-511C/T;rs16944) polymorphism, IL-1β serum levels, and renal function among Egyptian cases with T2DM. - Source: PubMed
Publication date: 2026/05/07
Zaki Maysaa El SayedSalem Eman Hosney MohammedElbaz Amro Abdel-HamidEssa Sara Ghaleb - Reliable molecular biomarkers for poststroke cognitive impairment (PSCI) remain limited. Using publicly available bulk transcriptomic and single-cell RNA-seq datasets from GEO, we investigated lactate metabolism- and pyroptosis-related signatures and developed a diagnostic model. Differential expression analysis, KEGG pathway enrichment, and weighted gene coexpression network analysis (WGCNA) were performed, followed by multialgorithm feature selection (LASSO, SVM-RFE, and random forest). A logistic regression classifier was trained in the discovery cohort and externally validated in an independent cohort. Glycolysis/lactate metabolism, HIF-1 signaling, and NOD-like receptor-related pathways were enriched in PSCI-associated samples, and key coexpression modules were strongly correlated with ischemic injury traits. Cross-model consensus identified LDHA, GSDMD, and CASP1 as hub genes, yielding an AUC of 0.912 (95% bootstrap CI: 0.841-0.983) in the training cohort and 0.885 (95% bootstrap CI: 0.798-0.972) in the validation cohort. Immune deconvolution and scRNA-seq validation suggested increased proinflammatory microglia-associated signals, with relatively higher LDHA expression in microglia than in neurons; cell-cell communication analysis highlighted inflammatory interactions including IL1B-IL1R1. Connectivity map (CMap) analysis nominated candidate compounds, and molecular docking predicted favorable binding between oxamate and LDHA (binding energy = -9.5 kcal/mol). Collectively, these findings propose a compact LDHA/GSDMD/CASP1 biomarker panel for PSCI diagnosis and provide hypothesis-generating therapeutic leads that warrant further experimental validation. - Source: PubMed
Publication date: 2026/05/06
Ge ShulongZhang QiyingLiu NingZheng XueyanXu HanZhang Li - » There is a poor understanding of the significance of biomarkers in the blood, synovial fluid, and tissue in patients with shoulder instability and posttraumatic osteoarthritis (PTOA). » Identification of biomarkers associated with injury severity in shoulder instability may provide prognostic information to help guide surgical treatment algorithms. » Current evidence suggests that the biomarkers of periostin, tumor necrosis factor-alpha, IL1B, and cartilage oligomeric matrix protein are associated with injury severity in patients with recurrent anterior shoulder instability. » There is limited information on genetic, transcriptomic, and protein biomarkers which may indicate individuals who are at more risk for development of shoulder instability. » An improved understanding of the local biomolecular tissue response to first-time and recurrent anterior shoulder instability may contribute to the development of novel therapeutic strategies for gene and protein targets to halt the early cascade of PTOA. - Source: PubMed
Publication date: 2026/05/12
Rooney Patrick WCorken ReillyWishman Mark DCall CoryBozoghlian MariaLane CarterColeman Mitchell CNepola James VPatterson Brendan MGalvin Joseph W - Platelet-rich fibrin (PRF) is extensively utilized to enhance localized tissue healing, a process that critically depends on the transient polarization of macrophages toward a pro-inflammatory phenotype. Given that PRF, like other blood clot derivatives, may intrinsically modulate macrophage behavior, we conducted a comprehensive screening assay to characterize the global macrophage response to PRF exposure. To this end, we employed two widely used monocytic cell lines-U937 (histiocytic lymphoma) and THP-1 (acute monocytic leukemia)-as models to investigate macrophage responses. Cells were exposed to lysates derived from PRF, and transcriptomic alterations were profiled using bulk RNA sequencing. Differential gene expression analysis was performed, with significance determined by an adjusted p-value threshold of <0.05. In U937-derived macrophages, gene expression profiling revealed a transcriptional signature consistent with inflammatory activation. Clustering of upregulated genes highlighted pathways associated with chemokine activity (e.g., CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL20, CCL23, CCL26, CXCL5, CXCL6, CXCL8, CXCL16, and PPBP), RAGE receptor binding (FPR1, S100A8, S100A9, and S100A12), IgG binding (FCGR1A, FCGR2A, FCGR2B, and FCGR3A), prostaglandin biosynthesis (CBR1, CD74, EDN1, FABP5, IL1B, MIF, PTGES, and PTGS1), and collagen catabolism (CTSL, FAP, MMP3, MMP7, MMP9, MMP12, MMP14, MMP19, and MRC2). In contrast, PRF exposure in THP-1 cells primarily enriched genes involved in steroid biosynthesis, suggesting a more limited or distinct response. These findings underscore U937 cells as a more responsive and appropriate bioassay for modeling inflammatory macrophage polarization in response to PRF. Moreover, the identified gene signatures recapitulate key aspects of early wound healing, providing a relevant platform for studying macrophage reactivation in chronic wound environments. - Source: PubMed
Publication date: 2026/04/22
Panahipour LaylaHuang XiaoyuZampino FrancescaMiron Richard JGruber Reinhard