S100A8, human, unlabelled
- Known as:
- S100A8, H. sapiens, unlabelled
- Catalog number:
- 201SA08_H
- Category:
- -
- Supplier:
- ProtEra
- Gene target:
- S100A8 human unlabelled
Related genes to: S100A8, human, unlabelled
- Gene:
- S100A8 NIH gene
- Name:
- S100 calcium binding protein A8
- Previous symbol:
- CAGA, CFAG
- Synonyms:
- P8, MRP8, 60B8AG, CGLA
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2018-05-02
Related products to: S100A8, human, unlabelled
Related articles to: S100A8, human, unlabelled
- Several cardiovascular diseases are associated with tumor development. But the mechanisms underlying how the hypertrophic heart promotes tumor progression remain unknown. Here, we show that extracellular vesicles from hypertrophic cardiomyocytes facilitate cancer progression. Following transverse aortic constriction to induce cardiac hypertrophy, 4T1-Luc cells are orthotopically implanted into mice. Concurrently, AC16 cells are treated with angiotensin II, and extracellular vesicles isolated from these cells are administered to BALB/c nude mice previously implanted with MDA-MB-231 cells in their mammary fat pads. Both transverse aortic constriction-operated mice and mice receiving extracellular vesicles from angiotensin II-treated AC16 cells exhibit accelerated breast cancer progression; however, treatment with GW4869, an extracellular-vesicles-release inhibitor, suppresses this effect. Transcriptome sequencing and mass spectrometry indicate that the expression of miR-362-5p, S100A7, and S100A8 is upregulated in these extracellular vesicles, which significantly boosts breast cancer cell proliferation, invasion, and migration. Importantly, miR-362-5p, S100A7, and S100A8 levels are elevated in plasma extracellular vesicles from patients with myocardial hypertrophy and are positively correlated with inflammatory indices. Our research identifies the specific factors in hypertrophic cardiomyocytes that drive tumor progression, laying a theoretical foundation for future targeted intervention and prevention. - Source: PubMed
Publication date: 2026/05/06
Chen WeiweiYao YutongXin BenkaiAn PeipeiDai YonghaoGao HanweiYang JingtongWang XiaoyuShi YueruZhu ZhouleiZhang NanWan YouzhongHe YuquanHu Xin - Salivary biomarkers are emerging as valuable, non-invasive tools in the field of bovine medicine. The calgranulins S100A8/A9 and S100A12 are major neutrophil-derived proteins reflecting innate immune activation. This study aimed to develop and validate a new immunoassay for S100A12 measurements and evaluate the dynamics of both calgranulins in cow saliva under physiological (peripartum) and pathological (lameness) conditions. An AlphaLISA immunoassay for S100A12 was developed and analytically validated, demonstrating high precision (intra- and inter-assay coefficients of variation (CVs) <15%), accuracy (mean recovery, 101.8%; linearity under dilution,R > 0.98) and high sensitivity (LLQ = 0.03 mg/L). Then, salivary concentrations of S100A12 and S100A8/A9 were measured in multiparous Holstein-Friesian cows around parturition (n = 48 samples) and in lame versus healthy cows (n = 24 samples). Both proteins exhibited significant increases at calving compared to pre- and postpartum values (p < 0.05) and were positively correlated with inflammatory biomarkers (haptoglobin and adenosine deaminase). S100A12 also was negatively correlated with antioxidants (CUPRAC, FRAP and TEAC). In lame cows, S100A12 and S100A8/A9 increased 2.4- and 3.25-fold respectively, compared with healthy controls (p < 0.05). Strong correlations were observed between S100A8/A9 and S100A12 in both conditions. These findings suggest that salivary S100A12 and S100A8/A9 are potential indicators of general inflammatory activation, being S100A12 also associated with oxidative stress. Overall, this supports further investigation to elucidate their potential as non-invasive biomarkers for assessing the health and welfare of dairy cows. - Source: PubMed
Publication date: 2026/04/19
Botía MVallejo-Mateo PEscribano DHevia-Méndez M LContreras-Aguilar M DCerón J JMartínez-Subiela SRubio C PMuñoz-Prieto A - Primary open-angle glaucoma (POAG) is a progressive optic neuropathy that leads to irreversible vision loss, primarily due to dysfunction of the trabecular meshwork (TM). Although impaired autophagy has been implicated in POAG pathogenesis, its molecular drivers remain poorly defined. This study systematically investigated autophagy-related genes (ATGs) in TM tissue from POAG patients. Transcriptomic datasets (GSE4316 and GSE27276) were analyzed to identify differentially expressed genes (DEGs). A curated list of autophagy-related genes (ATGs) from HADb and GeneCards was intersected with DEGs to identify differentially expressed ATGs (DEATGs). Functional analyses included Gene Ontology (GO) and KEGG pathway enrichment, protein-protein interaction (PPI) network construction, hub gene identification, immune cell infiltration profiling via single-sample gene set enrichment analysis (ssGSEA), and molecular docking to evaluate predicted interactions between latanoprost and hub proteins. A total of 990 DEGs were identified, including 15 DEATGs. Among these, S100A8 and S100A9 emerged as hub genes, exhibiting strong functional similarity and central roles within the PPI network. Enrichment analysis revealed significant involvement in autophagy regulation, tyrosine metabolism, and oxidative phosphorylation. Notably, molecular docking predicted high-affinity binding between latanoprost and S100A9. Immune profiling demonstrated significant alterations in both innate and adaptive immune cell populations, including a strong positive correlation between S100A9 expression and Th2 cell abundance. These findings suggest that S100A9 may act as a central regulator linking autophagy deficiency to immune dysregulation in POAG. Its predicted interaction with latanoprost highlights a potential molecular mechanism for pharmacologic modulation of TM homeostasis, supporting the therapeutic value of targeting S100A9-mediated autophagy-immune crosstalk in intraocular pressure control. - Source: PubMed
Publication date: 2026/03/11
Hu LiliPan ShaoxinChen GongLei MinAi MingLv XiangyunPan HaoningWang PengChang Rui - The host immune determinants that distinguish protective from life-threatening responses to influenza are poorly understood. Identifying drivers of immunopathology in the human lung is critical for developing potential therapies. - Source: PubMed
Publication date: 2026/03/16
Xiao KunCao YanHan ZhihaiDa QianFeng YunTian RongLuu Laurence Don WaiZhang LiLi XiaoyanWang RuijuanLi QiHu MeiAn FuchengLi XiangxinZhang FeiQiao ShubinNie QingrongJiang PingMa XiaHu YeWang KaifeiDuan ZhimeiLiu YangWang JiaxinXu WenjianYan PengGao XiangCao BinXie LixinWang Yi - BACKGROUND Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive malignancy with limited prognostic biomarkers and therapeutic targets. This study aims to develop a robust protein-based prognostic model and investigate the functional role of RAPTOR in HNSCC progression. MATERIAL AND METHODS Proteomic data from The Cancer Proteome Atlas and transcriptomic data from The Cancer Genome Atlas were integrated to identify prognosis-related proteins, and a multivariable Cox regression model was developed. Functional studies, including lentiviral knockdown, proliferation and invasion assays, RNA sequencing, and xenograft models, were conducted to evaluate the role of RAPTOR (encoded by the RPTOR gene). Since RAPTOR is an essential component of mTORC1 and lacks a direct inhibitor, the mTORC1 inhibitor rapamycin was used as a pharmacological surrogate to assess the therapeutic potential of targeting RAPTOR-mediated signaling. RESULTS A 7-protein prognostic model (CD45, RAPTOR, SETD2, MERIT40_pS29, HER3_pY1289, Hexokinase-I, and BETACATENIN) stratified patients into high- and low-risk groups with significantly different overall survival, and the risk score remained an independent prognostic factor. RAPTOR was markedly upregulated in HNSCC and correlated with immune infiltration. Functional assays revealed that RAPTOR silencing inhibited proliferation, migration, and invasion, suppressed PI3K/AKT/mTOR signaling and uPA expression, and upregulated both S100A8/A9 levels. Rapamycin treatment recapitulated these effects in vitro and in vivo. CONCLUSIONS This study identifies a novel protein-based prognostic model for HNSCC and demonstrates that RAPTOR promotes tumor progression through mTOR signaling and S100A8/A9-uPA regulation. Targeting RAPTOR-mediated pathways may offer new strategies for precision therapy in HNSCC. - Source: PubMed
Publication date: 2026/05/05
Fu ZhenzhenWang SongZheng HaoranWu HuadongLi TaoWang LihaoLi HongZhang Qiang