S10A9_HUMAN CFAG ELISA tesk kit
- Known as:
- S10A9_HUMAN CFAG Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17442
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- S10A9_HUMAN CFAG ELISA tesk kit
Related genes to: S10A9_HUMAN CFAG ELISA tesk kit
- 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
- 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: S10A9_HUMAN CFAG ELISA tesk kit
Related articles to: S10A9_HUMAN CFAG ELISA tesk kit
- Diabetic foot ulcer (DFU) affects approximately 25% of diabetic patients and represents the leading cause of non-traumatic lower extremity amputation. Neutrophil extracellular traps (NETs) contribute to chronic inflammation; however, their mechanistic role in DFU healing failure remains incompletely characterized. This study integrated bulk RNA sequencing (GSE143735, n = 9) and single-cell RNA sequencing (scRNA-seq; GSE165816, n = 11) datasets to investigate NET-related transcriptional programs. Differential expression analysis identified 96 differentially expressed genes, with significant NET pathway enrichment in non-healers (normalized enrichment score = 4.35, false discovery rate q < 0.001). Analysis of 33,654 single cells revealed elevated NET activity scores in neutrophils from non-healing wounds ( = 4.73 × 10). Four neutrophil subpopulations were identified, with the NETs-high subset expanded in non-healers (43.1% versus 15.4%). Cell-cell communication analysis demonstrated enhanced S100A8/A9-RAGE and IL1B-IL1R signaling in the non-healing state. A six-gene signature (S100A8, S100A9, MPO, ELANE, NCF1, HMGB1) achieved an area under the receiver operating characteristic curve of 0.750 for healing prediction under leave-one-out cross-validation. These findings implicate NET pathway activation as a potential driver of DFU healing impairment and identify candidate prognostic biomarkers warranting prospective validation. - Source: PubMed
Publication date: 2026/07/27
Li DazhiGu HaoyuXia ShiboYuan LiangxiBao JunminLu Qingsheng - Increased S100 calcium-binding protein A9 (S100A9)-related signals have been reported in selected hepatic and ocular inflammatory settings. This structured narrative review evaluates S100A9-related species as candidate participants in hepato-ocular crosstalk. Across human, ocular fluid, animal, and cellular studies, the available findings provide context-specific support for disease-associated hepatic expression and ocular responsiveness, with stronger evidence for selected local S100A9-Toll-like receptor 4 (TLR4)-associated effects than for S100A9-specific receptor for advanced glycation end products (RAGE) signaling. Clinical associations involving metabolic dysfunction-associated steatotic liver disease, diabetic retinopathy, chronic liver disease, dry eye disease, and uveitis are heterogeneous and confounded. Interpretation is further limited by the non-equivalence of S100A9, S100A8/A9, calprotectin, and higher-order complexes. Current evidence, therefore, suggests that S100A9-related species may serve as exploratory indicators of inflammatory activity or contribute to local inflammatory amplification in selected settings, rather than acting as established liver-derived causal signals. Future studies should prioritize analyte-specific measurement, source tracing, and selective perturbation. S100A9 is best regarded as a testable candidate node within a broader metabolic-inflammatory network. - Source: PubMed
Publication date: 2026/08/05
Wang PengLi YameiXia BohouLin YanTuo QinhuiLin LimeiPeng Qiuxian - Inflammatory bowel disease (IBD) and osteoporosis (OP) often co-occur, with IBD accelerating OP onset, though the underlying mechanisms remain unclear. - Source: PubMed
Publication date: 2026/08/12
Su YueLuo XiaohuiXu Haitao - Bacterial epididymo-orchitis, primarily driven by uropathogenic Escherichia coli (UPEC), is a major cause of inflammatory testicular injury and male infertility. While our previous study indicates that neutrophils are rapidly recruited to the immune-privileged testis to contain the infection, their excessive activation can paradoxically exacerbate tissue destruction. However, the specific cellular states and molecular mediators driving this injurious inflammatory response remain poorly defined. To address this gap, we utilized single-cell transcriptomics in a murine orchitis model to map the dynamic remodeling of the testicular neutrophil compartment. We identified a dominant pathogenic subpopulation (Cluster 0) that rapidly expands during acute infection and is characterized by robust S100a8 expression (accompanied by concomitant induction of its heterodimeric partner, S100a9). Flow cytometric and spatial analyses confirmed the marked accumulation of CD11bLy6GS100A8 neutrophils within damaged reproductive niches. Notably, pharmacological inhibition of the S100A8/S100A9 complex with paquinimod reduced this pathogenic neutrophil infiltration and preserved testicular architecture. Together, these findings identify S100A8 as a key marker and candidate contributor to neutrophil-mediated tissue injury, and suggest that this axis warrants further investigation as a targeted immunomodulatory strategy that may help preserve fertility during bacterial infections. - Source: PubMed
Publication date: 2026/08/11
Ma JinZhou ZhenyuWang Ming - To investigate the role and molecular mechanisms of the deacetylase SIRT6 in psoriasis and evaluate its potential as a therapeutic target for topical treatment. - Source: PubMed
Publication date: 2026/08/06
He MingjieGuo QingWang XiaofangHuang ZhongzhouZhou JingWang QingJiang YanyunXiong Hui