Rabbit Anti-Human CD120b
- Known as:
- Rabbit Antibody toHuman CD120b
- Catalog number:
- 129-10094
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CD120b
Related genes to: Rabbit Anti-Human CD120b
- Gene:
- TNFRSF1B NIH gene
- Name:
- TNF receptor superfamily member 1B
- Previous symbol:
- TNFR2
- Synonyms:
- TNFBR, TNFR80, TNF-R75, TNF-R-II, p75, CD120b
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2016-06-28
Related products to: Rabbit Anti-Human CD120b
Related articles to: Rabbit Anti-Human CD120b
- In multiple sclerosis (MS), spontaneous remyelination occurs in early disease; however, this process becomes inefficient over time, resulting in sustained neurodegeneration and clinical deterioration. It is known that global tumor necrosis factor receptor 2 (TNFR2) deletion in experimental autoimmune encephalomyelitis (EAE), the murine MS model, causes a severe nonremitting disease; however, the underlying mechanism is poorly understood. Here, through bulk and single nucleus RNA sequencing, we identify endothelial TNFR2 deletion as the driver of nonremitting disease, as it is sufficient to drive a severe nonremitting phenotype that closely mirrors global TNFR2 loss. Remyelination failure upon endothelial cell-specific TNFR2 ablation was also detected at the Cuprizone model of remyelination confirming its dominant role in central nervous system (CNS) repair. Notably, this effect was independent of immune cell influx or vascular permeability changes but associated with fibronectin overexpression and accumulation in demyelinating lesions. Fibronectin accumulation led to the sequestering of oligodendrocyte progenitor cells (OPCs) at the demyelination areas and prevented myelin repair. Therapeutically, systemic fibronectin inhibition restored regeneration and clinical remission, as well as prevented OPC accumulation at lesions, providing strong preclinical evidence for fibronectin-targeting therapies in MS and other demyelinating disorders. These findings establish endothelial cells as key regulators of the parenchymal environment permissive to remyelination and open avenues for MS treatment strategies focused on vascular-driven CNS regeneration. - Source: PubMed
Publication date: 2026/09/08
Nanou AikateriniApostolou-Karampelis KonstantinosTriantafyllidou VasilikiSakkou MariaRoumelioti FaniDenis Maria CKollias George - The core pathological features of Alzheimer's disease (AD) include Aβ plaques and neurofibrillary tangles, which collectively drive the neurodegenerative process. Meanwhile, the phagocytic function of microglia plays a dual role in AD: it attempts to clear pathological proteins such as Aβ, but its chronic activation may also exacerbate neuroinflammation and synaptic damage. This study integrated microarray data from AD cohorts in the Gene Expression Omnibus (GEO) database. Through differential expression analysis, protein-protein interaction network construction, and three machine learning algorithms (Least Absolute Shrinkage and Selection Operator, Support Vector Machine-Recursive Feature Elimination, and Extreme Gradient Boosting), key microglial phagocytosis-related signature genes were identified. Diagnostic models were subsequently developed and validated, with further investigation of immune infiltration patterns, regulatory networks, and molecular subtypes. Based on comprehensive analysis, this study identified five core signature genes (HLA-DPA1, IL4R, ITGAM, SPP1, TNFRSF1B) that form a highly accurate diagnostic model validated in independent cohorts. Immune infiltration analysis revealed significant increases in neutrophils and M2 macrophages in AD brains, with these genes showing strong correlations with immune cell abundance. The study further identified two molecular subtypes with distinct immune features, constructed regulatory networks, and predicted potential therapeutics including Tamibarotene. By integrating transcriptomics and machine learning, this study identifies key molecular features of microglial phagocytosis in AD, providing a novel diagnostic framework and insights into the immune mechanisms of the disease. - Source: PubMed
Chang HuiminLiu YunYang XiaojunHan Yanqing - Extended laying cycles in hens lead to declines in production performance, health status, and egg quality, which raises concerns about animal welfare and food safety. This study investigated the effects of dietary bile acids (BAs) supplementation on production performance and eggshell quality in late-phase laying hens. A total of 320 62-wk-old Hy-Line Gray laying hens were randomly assigned to four groups and fed a basal diet or a basal diet supplemented with 200, 500, or 800 mg/kg BAs for 6 wk. Dietary supplementation with 800 mg/kg BAs significantly reduced eggshell translucency grade, increased eggshell thickness and percentage, and decreased egg weight loss during storage. Transcriptomic analysis of the isthmus revealed that BAs downregulated matrix-degrading enzyme MMP9 and inflammatory regulator TNFRSF1B, while modulating extracellular matrix-related genes. HE staining of uterine tissue showed that there were a large number of vacuoles in the gland in the CON group, while in the 800 mg / kg BAs group, the cells in the gland were closely arranged without obvious vacuoles. TUNEL staining showed brown apoptotic positive cells in the CON group, while the apoptotic cells in the 800 mg/kg BAs group were significantly reduced. Moreover, BAs exerted beneficial effects by enhancing antioxidant capacity (T-AOC, SOD), inhibiting pro-inflammatory cytokines (IFN-γ, IL-1β), and promoting Ca²⁺ utilization within the uterus. Collectively, these findings demonstrate that dietary BAs, particularly at 800 mg/kg, effectively reduce eggshell translucency in aged laying hens. This improvement is associated with the preservation of shell membrane integrity via downregulation of ECM-degrading enzymes in the isthmus, and the enhancement of calcification through alleviation of oxidative stress and inflammation in the uterus. - Source: PubMed
Publication date: 2026/08/04
Zhu JiweiYang HaoZhu JianguoChen LeiWang JinYu HuiCao AizhiJia YiminHe Bin - The heterogeneity in associations between circulating fatty acids (FA) and mortality remained underexplored. Proteomics can profile the human physiological status. This study aimed to estimate interactions between FA and proteins in relation to mortality. We randomly divided 30,190 UK Biobank participants into train and test datasets. Multivariable Cox regression was utilized to assess the associations between FA and all-cause mortality and to explore proteome-wide interactions of FA in relation to mortality. Subgroup analyses were conducted to examine heterogeneity across varied protein levels. We also explored interactions between proteins and FA in relation to cause-specific mortality. We documented 3,345 deaths during 13.9 years of follow-up. MUFA-pct, Non-LA Omega-6 pct, Omega-6/Omega-3 ratio and SFA-pct were positively associated with all-cause mortality, while PUFA-pct, DHA-pct, LA-pct, and Omega-3-pct were negatively associated. We identified several robust interactions of proteins with MUFA-pct (n = 3), Omega-3-pct (n = 4), and Omega-6/Omega-3 ratio (n = 2). In subgroup analyses, individuals with high-level TNFRSF1B, MMP10, and CRHBP had higher all-cause mortality risks associated with MUFA-pct, while protective associations between Omega-3-pct and all-cause mortality were stronger among individuals with high-level TSPAN8, PLAU, ITGA5, and CEACAM1. Moreover, participants with high-level TSPAN8 and PLAU had higher risks of all-cause mortality with Omega-6/Omega-3 ratio. For cause-specific mortality, interaction and subgroup results were largely consistent with those of all-cause mortality. Our findings can provide new insights into heterogeneity in FA-mortality associations and highlight potential protein targets for personalized interventions across individuals with different physiological status. - Source: PubMed
Publication date: 2026/08/10
Qiao ZiyanWang XinruTao ChengzheLiao SijingLu JiaweiYuan YitingXu QiaoqiaoFan YunWang XuLu Chuncheng - Pneumococcal serotype 1 (sequence type 217) is a leading cause of invasive disease outbreaks in Sub-Saharan Africa, causing significant morbidity and mortality. Understanding the transmission dynamics of hypervirulent strains such as ST217 is key to developing therapies and vaccines that can reduce outbreak incidence. - Source: PubMed
Publication date: 2026/07/20
Beentjes DaanMurray JamesFrench NeilVipond CarolineXu RongKadioglu Aras