Mouse Anti-Human CD266
- Known as:
- Mouse Antibody toHuman CD266
- Catalog number:
- 129-10131
- Product Quantity:
- 25
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD266
Related genes to: Mouse Anti-Human CD266
- Gene:
- TNFRSF12A NIH gene
- Name:
- TNF receptor superfamily member 12A
- Previous symbol:
- -
- Synonyms:
- FN14, TweakR, CD266
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-20
- Date modifiied:
- 2016-06-28
Related products to: Mouse Anti-Human CD266
Related articles to: Mouse Anti-Human CD266
- Oral squamous cell carcinoma (OSCC) often arises from oral epithelial dysplasia (OED); however, the gene expression changes during OED progression and its microenvironment are not fully understood. This study used spatial transcriptomics to identify differentially expressed genes and microenvironmental alterations associated with malignant transformation of OED. A retrospective analysis of paired OSCC and OED samples was conducted at the Faculty of Dentistry, University of Toronto. A total of 24 paired progressing OED (OED-P) and 23 matched non-progressing OED (OED-NP) cases were examined using spatial transcriptomics in PanCK+ (epithelium) and PanCK- (stroma) regions. The analysis included differential gene expression, pathway analysis, and spatial deconvolution. Our results identified differentially expressed genes in OED-P compared with OED-NP and even more extensive changes between OED-P and matching OSCC. Pathway analysis supported the activation of immune pathways, ubiquitination, metabolic reprogramming, and matrix-remodeling signatures during progression. Functional validation shows that TNFRSF12A (Fn14) contributes to the molecular mechanisms underlying OED progression to OSCC. The OSCC microenvironment showed increased numbers of fibroblasts, neutrophils, monocytes, and mast cells compared with OED. We report a comprehensive transcriptional analysis of matched OED cases, and our results suggest that spatial profiling of OED can help identify unique and actionable gene signatures and microenvironmental changes that occur before oral malignant transformation. Implications: Our study identifies spatially resolved molecular alterations associated with oral cancer development and highlights Fn14 as a promising biomarker and therapeutic target for intercepting malignant transformation. - Source: PubMed
Publication date: 2026/09/29
Lavoie VincentDos Santos Erison SantanaJeong WillJeon James SFernandez Andrade JuanAli AimanMolska Graziella REsfandiari NajmehYeo Hui LingJurisica IgorChugh DeepikaLeong IonaBubola JustinBradley GraceMagalhaes Marco - Intestinal barrier dysfunction and mucus layer abnormalities are central features of inflammatory bowel disease, yet the epithelial mechanisms regulating goblet cell function remain incompletely understood. The TWEAK/Fn14 pathway is involved in intestinal inflammation, but its role in small intestinal epithelial responses, particularly in goblet cells, has not been fully clarified. In this study, we investigated TWEAK/Fn14 signaling using mouse small intestinal epithelial organoids. Fn14 was expressed in MUC2-positive cells in intestinal tissue, with staining preferentially observed toward the mucin-facing region. Fn14 staining was also observed in small intestinal epithelial organoids. TWEAK stimulation increased mRNA expression by approximately 1.56-fold and reduced mRNA expression to approximately 66% of control, without markedly affecting epithelial proliferation or stem cell markers. TWEAK did not significantly alter the PAS-positive mucin area or AB-PAS-defined mucin composition, whereas PGM34 staining showed a non-significant tendency to increase. TNF treatment reproduced some of the TWEAK-associated changes, including reduced mRNA expression and alterations in mucin-associated parameters, suggesting that TNF may contribute to some of the epithelial responses associated with TWEAK treatment. Treatment with an anti-TNF neutralizing antibody modified several TWEAK-associated responses, including changes in epithelial-associated gene expression and mucin-associated staining parameters. These findings suggest that TWEAK treatment is associated with goblet cell-related mucin responses in mouse small intestinal epithelial organoids, with possible involvement of TNF signaling. - Source: PubMed
Publication date: 2026/08/26
Tamaki ShunKono MasayukiArikawa SakuraHigashi YuiMaekawa TatsunoriHara YusukeTsujimoto TaizoKawakami FumitakaImai MotokiKurosaki YoshifumiNaito ShokichiIshii NaohitoIchikawa TakafumiKawashima Rei - Plasma and cerebrospinal fluid (CSF) protein biomarkers in amyotrophic lateral sclerosis (ALS) may provide insight into disease mechanisms and yield clinically useful biomarkers. - Source: PubMed
Pan LuHou CanSeitz ChristinaIngre CarolineHedman Åsa KLaffita JoseVu Trung NghiaPawitan YudiUllgren AbbeYazdani SolmazAndersson JohnJoyce Emily EChourpiliadis CharilaosLovik AnikóChen YanLewandowski Sebastian AFernandez-Capetillo OscarBarz MyriamSamuelsson KristinPress RayomandPiehl FredrikGraff CarolineMälarstig AndersFang Fang - The potential pathogenesis and reliable biomarkers of Bladder cancer (BC) remain to be explored. Ubiquitination plays a crucial role in BC progression, warranting the necessity to develop prognostic gene signatures. - Source: PubMed
Publication date: 2026/07/28
Li ZhibiaoYan TingHu ChuxianLu ZechaoZhang JiahaoWu XiujunChen YushuTang ZhichengZheng HanxiongHe ZhaohuiTang Fucai - Glioma stem cells (GSCs) drive tumor heterogeneity, therapy resistance, and immunosuppression. This study identified molecular subtypes of glioma based on stemness-related genes and validated a key hub gene through bioinformatics and experiments. A stemness gene set was compiled from single-cell data, GeneCards, and MSigDB. Consensus clustering (NMF) on 157 glioma samples from GSE4290 revealed two subtypes (C1 and C2), with C1 showing higher stemness scores. C1 exhibited enriched DNA repair, proliferation, and metabolic pathways, plus greater temozolomide (TMZ) resistance and M2 macrophage infiltration. WGCNA and differential expression identified 43 genes; machine learning (LASSO, SVM-RFE, RF) selected TNFRSF12A as the core hub gene. TNFRSF12A knockdown in GSCs inhibited proliferation and stemness markers (CD133, OLIG2, SOX2), enhanced TMZ sensitivity, and suppressed M2 macrophage polarization. In vivo, TNFRSF12A silencing reduced tumor growth and synergized with TMZ. TNFRSF12A represents a potential therapeutic target for aggressive gliomas. - Source: PubMed
Publication date: 2026/08/01
Sun ShengyuZhang BoChen PengfeiWu LiangNiu Zhanfeng