Ask about this productRelated genes to: CXCL6 antibody
- Gene:
- CXCL6 NIH gene
- Name:
- C-X-C motif chemokine ligand 6
- Previous symbol:
- SCYB6
- Synonyms:
- GCP-2, CKA-3
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2016-03-01
Related products to: CXCL6 antibody
Related articles to: CXCL6 antibody
- Asthma constitutes a widespread chronic respiratory disease with multifactorial origins, in which definitive genetic components remain incompletely understood. This investigation synthesized transcriptomic data and Mendelian randomization (MR) to delineate causative genes contributing to asthma predisposition. Evaluation of the GSE43696 cohort disclosed 267 genes displaying expression alterations between healthy controls (n = 20) and asthmatic cases (n = 88). MR methods discerned seven causal genes, consisting of six protective determinants (GPRIN3, SHISA2, DUSP5, FCER1A, USP36, and LGALS2; OR < 1) and one risk-associated determinant (CXCL6; OR > 1). Independent validation with the GSE63142 series verified pronounced suppression of five genes in asthma specimens. Functional enrichment studies connected these genes to immune-related cascades, including IL-17/NF-κB signal transduction and Th17 cell differentiation, alongside metabolic activities. Single-cell transcriptomic assessment of 32,809 cells exposed compartmentalized expression profiles: FCER1A and LGALS2 predominated in dendritic cells, DUSP5 in goblet cells, SHISA2 in ionocytes, and USP36 in T cells. Immune cell infiltration evaluation demonstrated shifted distributions of mast cells, eosinophils, and monocytes, exhibiting substantial linkages with immune mediators such as CCR5 and CXCL10. Transcription factor exploration recognized cisbp__M0561 as the predominant regulatory element. Connectivity Map-based interrogation nominated KI-8751, verrucarin-A, and homoharringtonine as plausible therapeutic candidates. This consolidated multiomics framework elucidates previously uncharacterized pathological processes and prospective treatment avenues for asthma. - Source: PubMed
Liu FangCui HongtaoMei YanLi KeyuXu YanLi ShumanYuan Chao - 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 - Knee osteoarthritis (KOA) is a degenerative bone and joint disease. Jingu Zhitong Gel (JGZTG) exhibits a promising therapeutic effect in the clinical treatment of knee osteoarthritis (KOA). However, the mechanism of JGZTG in treating KOA remains unclear. - Source: PubMed
Publication date: 2026/04/17
Li LuLiang YiyaoDong JingSu ZhenzhenXu XinyuWu ZiyinZhang XinzhuangLi JifengWang ZhenzhongLiu WenjunCao LiangXiao Wei - S100A12 as an indispensable molecular components inflammatory cytokines in human physiology. Notably, similar pathological mechanisms involving chronic low-grade inflammation are also observed in intervertebral disc degeneration (IVDD) and osteoporosis (OP), making the interplay between these diseases and inflammatory cytokines indisputable. Nevertheless, the precise identity of cytokines that concurrently fuel IVDD and OP remains elusive, hindering targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/04/09
Wang ZexinChen BinLiu ZhenchuanZhang YuanqiangHan Leixiang - The N6-methyladenosine (mA) reader YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) plays a critical role in the tumorigenesis of intrahepatic cholangiocarcinoma (ICC), but its function in the tumor immune microenvironment remains unclear. RNA sequencing analysis of human ICC samples revealed that, among mA-related regulators, YTHDF1 exhibited the most significant negative correlation with immune score. In multiple ICC mouse models, Ythdf1 overexpression enhanced the recruitment of myeloid-derived suppressor cells (MDSCs) and suppressed cytotoxic CD8 T cell responses, promoting ICC progression. Immunostaining of human ICC tissue microarray verified that high YTHDF1 protein expression was significantly associated with increased accumulation of MDSCs and decreased infiltration of CD8 T cells. Mechanistically, YTHDF1 bound to the mA site of FOSL2 mRNA and promoted the translation of FOSL2, a transcription factor driving cytokine CXCL6 expression. Consequently, elevated CXCL6 recruited and activated MDSCs by binding to its receptor CXCR2, leading to the dysfunction of CD8 T cells in ICCs. In addition, targeting YTHDF1 alongside blockade of its downstream chemokine pathway enhanced the efficacy of anti-PD-L1 treatment in preclinical ICC mouse models, serving a promising strategy for improving immunotherapy efficacy in ICC. - Source: PubMed
Publication date: 2026/04/13
Luo LiLiu ZiqinSong ZiminZhang DongLiang CongFang FeiLei KaiWang LinaChen WeikangShen ShunliKuang MingLi XiaoxingYu JunWang ShiyanXu Lixia