Anti-Mouse CD126 PE 25 ug
- Known as:
- Antibody toMouse CD126 PE 25 ug
- Catalog number:
- 12-1261-80
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD126 25
Related genes to: Anti-Mouse CD126 PE 25 ug
- Gene:
- IL6R NIH gene
- Name:
- interleukin 6 receptor
- Previous symbol:
- -
- Synonyms:
- CD126
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: Anti-Mouse CD126 PE 25 ug
Related articles to: Anti-Mouse CD126 PE 25 ug
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Publication date: 2026/07/20
Tian RuoxiSha ZiyueZhang ShashaGong MiaoWu JianhuaLu JuntaoGuo WeiZheng ZhaoxuGuo Zhanjun - A central challenge in computational geroscience is to distinguish molecular quantities that mortality from those that it. Epigenetic clocks and aging biomarkers are increasingly used as if they were that mechanism, yet this is rarely tested directly. This distinction also bears on competing theories of aging: damage/reliability (A), hyperfunction/mTOR-IIS (B-1), and information loss (B-2). Although individual aging proteins have been tested piecemeal, no study has asked, in one framework, what fraction of mortality is measurable, whether it is causal, and whether it is reversible. Using only public, de-identified data, we evaluate this three ways. First, a Markov model of hallmark-load dynamics with death as an absorbing state, fitted by Bayesian inference through a joint biomarker-and-mortality likelihood to NHANES with linked mortality (n=23,844) and replicated in the Health and Retirement Study (HRS), decomposes Gompertz acceleration into (measured-biomarker-driven) and components. Second, a positive-control-calibrated, two-platform cis-pQTL Mendelian-randomization and colocalization design (UKB-PPP, de-CODE) against parental-lifespan GWAS tests whether the latent's measurable components are causal. Third, a clock battery (Horvath, chronological; DamAge, causality-enriched damage) tests reversibility in cellular reprogramming. Within the model, ∼92% of Gompertz acceleration is assigned to a latent component not captured by measured blood-biomarker axes (NHANES 92.5%, HRS 91.6%); the latent is partly encoded in DNA-methylation signatures but not transcription. The known causal proteins are detected (LPA p=9×10⁻¹²; IL6R p=2.8×10⁻⁵), yet the latent's components, across inflammatory, renal and growth-signalling (IGFBP3, IGF-1) axes, are null and do not colocalize on either platform. Reprogramming reverses the chronological clock (-11 to -22 yr) but not the causality-enriched damage clock. The model-inferred mortality-driving component is largely latent to accessible biomarkers; its measurable molecular proxies show no supported causal effect where the design detects known causes; and the causality-enriched damage-clock signal is resistant to partial reprogramming. - Source: PubMed
Publication date: 2026/07/09
Tanigawa MasatoIwaki Takafumi - Natural killer (NK) cells contribute to the development of Rheumatoid Arthritis (RA). Increased expression of programmed cell death protein 1 (PD-1), encoded by the PDCD1 gene, indicates NK cell exhaustion, a process that may be influenced by microRNAs (miRNAs). In this study, we examined PD-1 expression on NK cells from RA patients and evaluated whether miRNAs modulate this pathway. Although antibiotics are critical for treating infections, they can provoke harmful immune responses by releasing bacterial components that overstimulate the immune system. Such responses may lead to excessive inflammation or cytokine storms. To address this risk, we assessed the immune safety of a newly designed chimeric endolysin, ZAM-MSC, and compared its effects with traditional antibiotics using transcriptomic, proteomic, and computational analyses. We analyzed public gene and protein expression datasets from antibiotic-treated human cells and performed in silico studies on ZAM-MSC. Differential expression analysis and pathway enrichment were conducted, alongside structural modeling of the endolysin and its predicted interactions with immune receptors. Antibiotic treatment strongly activated inflammatory genes and pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK). In contrast, ZAM-MSC minimally affected immune-related gene expression, with downregulation of interleukin-6 receptor (IL6R) and tumor necrosis factor receptor 1A (TNFRSF1A). Structural modeling showed weak interactions with Toll-like receptors, and epitope analysis predicted low immunogenicity. These results suggest ZAM-MSC may offer a safer antimicrobial alternative, though all protein-level findings are based on computational predictions and require experimental validation. - Source: PubMed
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Publication date: 2026/06/25
Gan XinxinYan RuiYang BoWang JieGuo JianmingWang XiangHu XiaoyiWang LinhuiLiu Bing - Immune checkpoint inhibitor-induced inflammatory arthritis (ICI-IA) is an immune-related adverse event (irAE) following treatment with PD-1, PD-L1, or CTLA-4 inhibitors in patients with cancer. In this issue of the JCI, Ma and colleagues identified a subset of regulatory T cells (Tregs) that coexpress CD137 and IL-6 receptor (IL6R), termed atypical Tregs (AtpTregs), which are selectively enriched in patients with ICI-IA. Functionally, AtpTregs exhibited reduced suppressive capacity and a Th17-like proinflammatory phenotype. Notably, these cells were associated with more severe arthritis, yet improved cancer outcomes, suggesting a potential role in tumor control. The anti-IL6R therapy tocilizumab, administered as an off-label intervention for ICI-IA, reduced AtpTreg abundance and alleviated arthritis while maintaining antitumor immunity in a small cohort of patients with new-onset ICI-IA. Thus, anti-IL6R could be a targeted approach to manage ICI-IA and potentially other irAEs involving AtpTregs. - Source: PubMed
Publication date: 2026/07/01
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