S100A9, human, recombinant, full length
- Known as:
- S100A9, H. sapiens, Rec., length
- Catalog number:
- G02S1A09
- Product Quantity:
- 10 mg
- Category:
- -
- Supplier:
- Giotto Biotech
- Gene target:
- S100A9 human recombinant full length
Related genes to: S100A9, human, recombinant, full length
- 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, human, recombinant, full length
Related articles to: S100A9, human, recombinant, full length
- Infections are frequent in critically ill patients with earthquake-associated crush injury (CI) and contribute to poor outcomes, yet the immune pathways underlying posttrauma susceptibility remain poorly defined. We investigated longitudinal changes in damage-associated molecular pattern (DAMP)/PAMP sensing and downstream inflammatory programs in CI patients requiring intensive care. - Source: PubMed
Yuksel Recep CivanDemir Busra SenizHouran Mohammad AhmadAsan MineTemel SahinKaynar Ahmet SafaUlger BirkanTalih TutkunEsmaoglu AliyeSungur MuratGündoğan KürşatEken Ahmet - Renal cell carcinoma (RCC) is the most common malignancy of the urinary system, characterized by high incidence, mortality, and resistance to therapy. Its molecular heterogeneity presents challenges for effective precision treatment. RCC is highly heterogeneous, yet treatment guidelines rely predominantly on kidney renal clear cell carcinoma (KIRC) studies, neglecting other molecular subtypes, which limits therapy personalization for non-KIRC patients. This study aimed to explore the role of small ubiquitin-like modifier (SUMOylation)-associated genes in the progression and prognosis of RCC and its subtypes. We identified 298 SUMOylation-associated differentially expressed genes (DEGs), including 151 RCC-specific genes after excluding expression changes attributable to RCC subtype-specific variation. Ten core genes (, , , , , , , , , and ) were identified, with expression not only discriminates tumor from normal tissue but also separates KIRC from KICH/KIRP, proposing as a potential second-step biomarker for KIRC identification on top of traditional histology. Inter-subtype RCC heterogeneity represented a key factor limiting predictive performance of the six prognostic signature genes (, , , , and ). Its 5-year AUC exceeded 0.7 for every individual RCC subtype in the TCGA training cohort, with pooled 5-year AUCs of 0.61 (TCGA training cohort) and 0.67 (independent PCAWG validation cohort). The prognostic risk model demonstrated strong predictive performance, with a C-index of 0.791 before calibration and 0.774 after calibration. Importantly, the C-index remained above 0.75 throughout the 60-month follow-up period, indicating stable and robust long-term prognostic accuracy. High-risk patients exhibited greater immune cell infiltration, indicating potential for immunotherapy. Following secondary screening, three RCC cell lines (BFTC909, CAKI1, and CAL54) and five target genes (, , , and ) were identified as optimal candidates for subsequent mechanistic investigations. This study uncovers the prognostic and functional relevance of SUMOylation in RCC and offers a novel framework for biomarker development, therapeutic targeting, and immunotherapeutic stratification. - Source: PubMed
Publication date: 2026/07/23
Zhang XiaoboLi ZhimingLin RuoxinYang SupingSun XiaohuiChen Shicheng - Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids, immune cells, and fibrotic tissue within the arterial wall. Among the immune cells that drive this process, macrophages play a central role by mediating both inflammatory activation and tissue repair. Their polarization into either pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes determines whether plaque progression or stabilization occurs. S100 proteins, particularly S100A8, S100A9, and S100A12, are critical regulators of macrophage function in atherosclerosis. Acting as damage-associated molecular patterns, these calcium-binding proteins interact with receptors such as receptor for advanced glycation end products (RAGE) and toll-like receptor (TLR)-4 to sustain inflammatory signaling, promote oxidative stress, and amplify cytokine production within atherosclerotic plaques. Elevated S100 protein levels correlate with increased macrophage infiltration, plaque instability, and heightened cardiovascular risk. Understanding how S100 proteins influence macrophage polarization offers new insights into the mechanisms underlying chronic vascular inflammation. Targeting the S100A8/A9 and S100A12 pathways represents a promising therapeutic strategy to mitigate macrophage-driven inflammation and improve plaque stability. Approaches such as inhibition of S100 protein-receptor interactions, suppression of downstream reactive oxygen species production, and modulation of macrophage polarization toward the M2 phenotype have shown potential in experimental models. This narrative review explores the roles of macrophages in atherosclerosis, the involvement of S100 proteins in both disease progression and macrophage polarization, and the therapeutic implications of targeting S100 protein-mediated immune responses. Together, these findings highlight S100 proteins as a therapeutic target modulating macrophage polarization to attenuate atherosclerotic plaque vulnerability. - Source: PubMed
Publication date: 2026/07/30
Kulkarni Atreya JRai Vikrant - Research demonstrates that pyroptosis is a critical factor in the progression of cardiovascular diseases and their related complications. Nevertheless, the precise association between this particular cell death process and the pathophysiological characteristics of atrial fibrillation (AF) remains uncertain. This exploratory study investigates the association between pyroptosis-related genes (PRGs), predicted immune-cell enrichment, and AF using a systems biology approach. Two datasets obtained from the Gene Expression Omnibus, along with a dataset from GeneCards pertaining to pyroptosis-related genes (PRGs), were utilized in this study. Following this, 18 AF-PRGs acquired from the GSE41177 dataset and PRGs were analyzed for functional enrichment using Gene Ontology (GO) annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and gene set enrichment analysis (GSEA). Subsequently, the validation dataset was employed to assess the 18 AF-PRGs, leading to the identification of seven candidate genes for exploratory validation. Then, interaction networks were developed to elucidate potential regulatory relationships among PRGs, miRNAs, transcription factors, and drugs. Finally, single-sample GSEA was used to estimate predicted immune-cell enrichment in AF. The KEGG pathway analysis indicated that AF-related PRGs are significantly enriched in pathways linked to NOD-like receptor signaling, lipid metabolism, and bacterial infection, highlighting the potential role of inflammation in the pathogenesis of AF. After validation, we identified seven additional reliable genes: , , , , , , and . Additionally, 177 miRNAs were predicted to regulate these seven genes, while 50 transcription factors (TFs) were identified to regulate six of them, and 38 drugs were predicted to target six genes as hypothesis-generating interactions. In assessing predicted immune-cell enrichment, we observed significant differences between AF and sinus rhythm atrial tissues. This exploratory study suggests that pyroptosis-related inflammatory gene signatures may be associated with AF and provides hypotheses for future mechanistic and translational validation. - Source: PubMed
Publication date: 2026/07/24
Zhang JunhaoMa YuweiChen BoyangYu Li - Human mesenchymal stromal cells (hMSCs) remain the most clinically advanced adult stem cell source; however, their therapeutic potential is limited by rapid replicative senescence during ex vivo expansion. Replicative senescence in hMSCs is characterized by cell cycle arrest, acquisition of senescence-associated β-galactosidase (SA-β-Gal) activity, and secretion of the senescence-associated secretory phenotype (SASP) factors. - Source: PubMed
Publication date: 2026/07/30
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