S100A9 _ Calgranulin_B _ MRP14
- Known as:
- S100A9 _ Calgranulin_B _ MRP14
- Catalog number:
- NBP1-40815
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- S100A9 _ Calgranulin_B MRP14
Related genes to: S100A9 _ Calgranulin_B _ MRP14
- Gene:
- S100A9 NIH gene
- Name:
- S100 calcium binding protein A9
- Previous symbol:
- CAGB, CFAG
- Synonyms:
- P14, MIF, NIF, LIAG, MRP14, MAC387, 60B8AG, CGLB
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2018-05-02
Related products to: S100A9 _ Calgranulin_B _ MRP14
Related articles to: S100A9 _ Calgranulin_B _ MRP14
- Vesicular cutaneous lupus erythematosus (VCLE) is a rare autoimmune disease in dogs and is considered the canine counterpart of human subacute cutaneous lupus erythematosus (SCLE). However, the molecular mechanisms underlying VCLE remain incompletely defined. - Source: PubMed
Publication date: 2026/05/11
Keating TreasaStranahan LaurenWiener DominiqueKeating M KellyLeon RenatoBanovic Frane - Chronic cadmium chloride (CC) exposure is associated with diverse toxicological outcomes, yet its potential role in the pathogenesis of ankylosing spondylitis (AS) remains unclear. This study employed a network toxicology framework to computationally elucidate the potential molecular mechanisms linking CC exposure to AS. AS-associated differentially expressed genes (DEGs) were identified from the GSE73754 dataset. Potential CC toxicity targets were retrieved from the Comparative Toxicogenomics Database (CTD). Overlapping genes were subjected to functional enrichment analysis, protein-protein interaction (PPI) network construction, and identification of core targets using multiple machine learning algorithms (LASSO, SVM, random forest, and XGBoost). A predictive nomogram was developed. Pathway activity dysregulation was assessed via Gene Set Variation Analysis (GSVA), and immune cell infiltration patterns were evaluated using the MCPcounter method. Additionally, two-sample Mendelian randomization (MR) analysis was performed to evaluate the causal relationship between the core target ETFA and AS, and in silico knockout of ETFA was conducted using single-cell RNA-seq data (GSE194315) to assess its regulatory impact. We identified 45 shared targets between putative CC toxicity and AS-associated DEGs. Enrichment analysis revealed their significant involvement in cytokine-mediated signaling, immune response, necroptosis, and the HIF-1 signaling pathway. PPI network analysis highlighted key hub proteins, including TNF, STAT3, and CXCL8. Machine learning models prioritized ZFC3H1, SCRN1, and ETFA as core toxicity-related targets, and the constructed nomogram demonstrated high predictive accuracy. In vitro validation in a HFLS chronic CC exposure model confirmed significant dysregulation of these core targets, with ZFC3H1 expression suppressed and SCRN1 and ETFA markedly upregulated. GSVA indicated a downregulation of several immune-related pathways in AS. Immune infiltration analysis showed altered abundances of cytotoxic lymphocytes, monocytes, and neutrophils. Correlation analysis linked the core targets to dysregulated pathways, particularly associating ZFC3H1 with humoral immune response and osteoclast differentiation. MR analysis indicated that ETFA is a potential risk factor for AS, with the inverse variance weighted method showing a nominally significant association. Virtual knockout of ETFA in AS single‑cell data led to substantial upregulation of immune-related genes, including S100A8, S100A9, S100A12, and multiple HLA class II genes, and enriched pathways such as antigen processing and presentation and phagosome. This study suggests that chronic CC exposure may exacerbate AS pathogenesis by perturbing immune-inflammatory pathways and altering immune cell infiltration. The core targets identified (ZFC3H1, SCRN1, ETFA) offer novel mechanistic insights into this link, with MR and knockout analyses further supporting ETFA as a causal risk factor involved in immune dysregulation, thereby highlighting the need for further experimental validation. - Source: PubMed
Publication date: 2026/05/11
Liu ZhuchenXue ZhiruiSong HanbingChen QipengZhang JingwenWang Geqiang - This study investigates host-pathogen interactions by comparing RNA profiles in plasma extracellular vesicles (EVs) from patients with severe sepsis or meningitis caused by with profiles from patients with systemic infections. At hospital admission both bacteria may present with similar symptoms, making early differentiation difficult. We have focused on EVs, as they function as active mediators of intercellular communication in the circulation. - Source: PubMed
Publication date: 2026/04/24
Brusletto Berit SletbakkHaug Kari Bente FossOlsen Iselin SandnesKaarbø MariOlstad Ole KristofferAspelin TrudeAmundsen Erik KoldbergBrandtzaeg PetterØvstebø Reidun - High-grade serous ovarian cancer (HGSOC) exhibits homologous recombination deficiency (HRD), but its impact on the immune microenvironment remains unclear. Using single-cell RNA sequencing, spatial transcriptomic inference, and survival analyses, we characterized 166,895 macrophages across HRD subtypes: functional BRCA1/2 inactivation (FBI), HRD-Del (deletions), and HRD-Dup (duplications). FBI macrophages showed lipid metabolism enrichment (S100A8, CD36), HRD-Del macrophages upregulated antigen presentation (HLA-DQA1, HLA-DPB1), and HRD-Dup macrophages displayed interferon-stimulated gene expression (ISG15, MX1). Six macrophage subtypes (C1Q, FCN1, MARCO, MKI67, MMP9, S100A9) exhibited distinct spatial distributions and functions. MKI67+ macrophages correlated with improved survival, while C1Q + subsets predicted worse outcomes. HRD-Dup tumors with high macrophage signatures had better survival, suggesting a favorable immune landscape. Our findings reveal HRD-driven macrophage reprogramming as a key determinant of immune microenvironment composition and clinical outcomes, supporting HRD-specific macrophage-targeted therapies for HGSOC. - Source: PubMed
Lan HuaXu FangLi LinshuangWei XinLi Minghua - Microglia are key regulators of neuroinflammation and neuronal survival after ischemic stroke. Emerging single-cell, transcriptomic, and metabolic studies show that ischemia induces rapid microglial reprogramming toward pro-inflammatory states that exacerbate neuronal death, oxidative stress, blood-brain barrier (BBB) disruption, and white-matter injury. Multiple pathways, including TLR4/NF-κB, NLRP3 inflammasome activation, Notch1-JAK/STAT signaling, epigenetic modulators such as HDAC3 and METTL14, and metabolic shifts involving AMPK/mTOR/HIF1α, collectively shape post-stroke microglial polarization. High-altitude hypoxia elicits similar inflammatory responses, activating microglia through RAGE-MAPK/NFκB signaling, CX3CL1/CX3CR1-dependent synaptic pruning, mitochondrial dysfunction, and lactate-mediated chromatin changes, highlighting hypoxia as a convergent driver of neuroinflammation. Modulating microglial activity, therefore, represents a promising therapeutic strategy. A wide range of natural compounds (e.g., curcumin, acteoside, astagaloside IV, artemisinin), synthetic agents (e.g., DBZ, resolvin D1), and cellular/molecular cellular interventions (e.g., rhFGF21, S100A9 inhibition, RBM3 induction) have shown efficacy in reducing inflammation, preserving BBB integrity, improving mitochondrial function, and promoting M2-like reparative phenotypes in preclinical models. Advances in understanding microglial subtypes, including CH25H, OASL, CD11c, and antioxidant Prdx1-enriched populations, further highlight their dynamic roles across injury and repair. This review presents current insights into microglial signalling, epigenetic and metabolic regulation, and therapeutic targeting in ischemic stroke, integrating parallel insights from high-altitude hypoxia. Together, these prospectives illuminate microglia as crucial mediators of neurovascular injury and recovery, and highlight opportunities for translating microglia-directed therapies into clinical interventions. - Source: PubMed
Publication date: 2026/05/06
Khan ShafaSultan ArmiyaSadik MohdAshraf Mohammad Zahid