I-TAC CXCL11, Human
- Known as:
- I-TAC CXCL11, Human
- Catalog number:
- Z03060-10
- Product Quantity:
- 10,0ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- I-TAC CXCL11 Human
Related genes to: I-TAC CXCL11, Human
- Gene:
- CXCL11 NIH gene
- Name:
- C-X-C motif chemokine ligand 11
- Previous symbol:
- SCYB9B, SCYB11
- Synonyms:
- H174, b-R1, I-TAC, IP-9
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-23
- Date modifiied:
- 2016-10-05
- Gene:
- SDCBP2 NIH gene
- Name:
- syndecan binding protein 2
- Previous symbol:
- -
- Synonyms:
- ST-2, SITAC18
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-17
- Date modifiied:
- 2015-12-16
Related products to: I-TAC CXCL11, Human
Related articles to: I-TAC CXCL11, Human
- The combination of antiangiogenic therapy with immune checkpoint blockade has demonstrated significant clinical benefits in various cancers, however, the precise mechanisms of action on the immune system are not fully understood. In particular, the early intratumoral immune responses induced by angiogenesis inhibition remain unclear. - Source: PubMed
Publication date: 2026/06/22
Geindreau MannonPignol CassandreCoënon LoïsVarin AlexisRacoeur CindyMilian LylouRoger NolwennChalmin FannyVernet ThibaultAlibert LineBellaye Pierre-SimonThibaudin MarionLouis CynthiaWicks IanTruntzer CarolineBoidot RomainPaul CatherineLamarthée BaptisteVegran FrederiqueGhiringhelli FrancoisBruchard Mélanie - The development of vaccines against Mycoplasma ovipneumoniae (MO) and the screening of novel therapeutic agents are hindered by the lack of a stable animal model for evaluation. Hu sheep, as a predominant breed in intensive farming systems, are highly susceptible to MO infection. Therefore, we established a MO infection model in Hu sheep to investigate the reasons for their susceptibility to MO. We collected tissue samples from the lung junction at the interface between diseased and healthy areas for pathological examination and transcriptomic analysis. Differentially expressed genes were screened and subjected to functional enrichment analysis, enabling an in-depth discussion of the mechanisms by which MO damages the lungs of Hu sheep. The study found that following infection with MO, Hu sheep exhibit a gradual rise in body temperature during the initial phase of infection. After several days of persistent fever, the temperature gradually returns to normal, while body weight shows a downward trend. Twenty-one days after infection with MO, hepatization of lung tissue was observed in the right apical lobe of the lung in Hu sheep. Histopathological sections from the lesion-control interface revealed thickened alveolar septa with extensive infiltration of red blood cells and inflammatory cells. Transcriptome sequencing identified 899 differentially expressed genes (|log2(Fold Change)| ≥ 1, padj≤ 0.05), comprising 535 upregulated genes and 364 downregulated genes. GO enrichment analysis indicates that the core functions of differentially expressed genes are concentrated in two biological processes: immune system processes and immune responses. KEGG enrichment analysis revealed that differentially expressed genes were significantly enriched across 28 distinct signaling pathways, identifying multiple key metabolic pathways associated with MO infection. These primarily encompassed the IL-17 signaling pathway, Toll-like receptor signaling pathway, NF-κB signaling pathway, TNF-α signaling pathway, and natural killer cell-mediated cytotoxicity pathways. We have additionally identified multiple genes associated with MO infection, including CCL19, CCL20, TNFSF11, CXCL8, CXCL11, CCR10, CSF3, IL2RA, CXCL1, CD40, BBOX1, and BPIFB1. These discoveries lay the groundwork for establishing MO infection models and investigating the mechanisms underlying sheep susceptibility. - Source: PubMed
Publication date: 2026/06/16
Zhao GuangxinCheng GuojieLiu WenjunGuo KepengSun YanmingZhang Yanbing - Stem cell-derived organoids are promising platforms for therapeutic screening in inflammatory bowel disease (IBD), but identifying functional organoid readouts with translational utility is challenging. Colon epithelial organoids from patients with ulcerative colitis (UC) overexpress chemokines CXCL1, CXCL11, CCL2, and CCL28, yet whether these inflammatory signatures correlate with disease activity and treatment response is unknown. This short report investigates whether organoid-retained chemokines correlate with disease activity and therapeutic outcomes. - Source: PubMed
Publication date: 2026/05/27
Alake SanmiKadam AnilJester TraciMaynard Craig LOjo Babajide A - Porokeratosis (PK) encompasses genetically heterogeneous keratinization disorders, with disseminated superficial actinic porokeratosis (DSAP) and porokeratosis ptychotropica (PPt) as distinct subtypes. Although MVK is a known causative gene, how different variants drive distinct phenotypes remains unclear. Through whole-exome sequencing of two DSAP patients, we identified an MVK variant (c.439G > A, p.Ala147Thr) cataloged as likely pathogenic in ClinVar yet uncharacterized functionally in DSAP keratinocytes. A previously reported PPt-associated variant (c.64G > A) was included for comparison. We established HaCaT cells stably overexpressing each mutant via lentiviral transduction and validated expression by qPCR and Western blot. Integrated transcriptomic and proteomic analyses identified differentially expressed genes (DEGs) and proteins (DEPs) across MVK439 versus control, MVK64 versus control, and MVK439 versus MVK64 groups, followed by GO and KEGG enrichment. Transcriptomic profiling revealed 231, 1,849, and 2,329 DEGs in the respective comparisons. Proteomic screening identified 2,673 DEPs, with 42 shared across all groups, 77 specifically associated with c.439G > A, and 832 linked to c.64G > A. Integrated analysis suggested IL12A and pIgR as potential contributors to c.439G > A-driven DSAP, while CXCL11, CXCL9, and TNFRSF12A may mediate c.64G > A-induced PPt. These findings offer new insights into MVK function and PK pathogenesis, warranting validation in larger cohorts. - Source: PubMed
Publication date: 2026/06/03
Lai ShuqinZhu WenjieLin ChunliGuo ZimengChen ShiqiXie LangLiu JieZeng ZhaolinYou CongLi Longnian - Vitiligo is a skin disease characterized by the loss of skin melanocytes, featuring the dual pathology of melanocyte damage due to oxidative stress and immune-mediated inflammation, which ultimately classifies it as an autoimmune condition. Sappanone A (SA), isolated from Caesalpinia sappan L., exhibits notable anti-oxidative stress and anti-inflammatory activity in various diseases. However, its potential effects and mechanisms in vitiligo remain uninvestigated. This study was designed to investigate the effects of SA on melanocytes and keratinocytes under oxidative stress and to evaluate its therapeutic potential in the monobenzone-induced vitiligo model. In vitro, SA protected PIG1 cells from HO-induced cytotoxicity and suppressed HMGB1 expression, nuclear export, and extracellular release. Furthermore, SA reduced HMGB1-induced overexpression of inflammatory cytokines in HaCaT cells, including CXCL8, CXCL9, CXCL10, CXCL11, and TNF-α. In vivo, SA administration alleviated monobenzone-induced depigmentation and CD8 T-cell infiltration in C57BL/6 mice. Transcriptomic analysis, protein-protein interaction network construction, and molecular docking revealed that Wnt5a may be a potential target of SA, and SA significantly reversed monobenzone-induced Wnt5a expression and activation of noncanonical Wnt signaling. Overall, SA effectively attenuated the HMGB1-mediated inflammatory response in keratinocytes. Furthermore, it exerted repigmentation effects in monobenzone-induced vitiligo mice via inhibiting the Wnt5a-mediated noncanonical Wnt signaling pathway. These results suggest that SA is a promising therapeutic candidate for vitiligo. - Source: PubMed
Publication date: 2026/06/02
Xu MingmingDing MeilinLi RuiZhang HejuanRen FeifeiLi HongyangZhang Wei