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
- Neuroendocrine prostate cancer (NEPC) is an increasingly recognized, highly aggressive disease variant with no actionable therapeutic targets and a life expectancy of 7 months or less. Using a transgenic mouse model, we now show that early stages of NEPC are associated with increased intraprostatic recruitment of Ly6G polymorphonuclear neutrophils (PMN) and reduced infiltration of CD8 T cells. This coincided with expansive transcriptional changes of increased cell viability and cell migration, as well as upregulation of multiple neuronal mediators with the neuropeptide, Neuromedin U (NMU) as the top hit (Z score = 4.34; FDR < 5%; p = 3.62 × 10). Analysis of a large cohort of human patient samples revealed that NMU was highly expressed in early and late stage prostate cancer, preferentially segregating with AR/NE metastases. Exposure of PMN to recombinant NMU was sufficient to stimulate cell migration, inflammatory gene expression with increased levels of the cytokine-like alarmin, S100A9 and suppression of T cell proliferation. Genetic or pharmacological targeting of NMU/S100A9 signaling inhibited NEPC growth, reinvigorated an intratumoral immune microenvironment via recruitment of tumor antigen-specific CD8 T cells with 'stem-like' (TCF1/PD1) and cytotoxic (GrzB/KLRG1) properties and enhanced the activity of therapeutic immune checkpoint inhibition, in vivo. Therefore, NMU 'innervation' drives myeloid immunosuppression in NEPC and provides a therapeutic target to restore sensitivity to immunotherapy in this highly refractory malignancy. - Source: PubMed
Publication date: 2026/09/01
Perego MichelaMadzo JozefKossenkov Andrew VAtilgan F CansuTazzari MarcellaTumedei Maria MaddalenaLimarzi FrancescoLolli CristianGurioli GiorgiaFatatis AlessandroIacocca Mary VPetrelli Nicholas JJacobi Justine JGoodrich David WLanguino Lucia RAltieri Dario C - - Source: PubMed
- Photobiomodulation (PBM) modulates inflammation and promotes tissue repair. S100A8/A9 is a neutrophil-derived calcium-binding heterodimer that acts as a pro‑inflammatory damage‑associated molecular pattern, serving as a biomarker of inflammation. This study aimed to evaluate the effects of PBM at 660 nm and 808 nm wavelengths on S100A8/A9 levels in pulp blood (PB) and gingival crevicular fluid (GCF) in patients with symptomatic irreversible pulpitis (SIP). Patients diagnosed with SIP were block-randomised into three groups: Group 1 received 660 nm PBM (n = 14), Group 2 received 808 nm PBM (n = 13), and Group 3 received sham irradiation (n = 8). PB and GCF samples were collected pre- and post-irradiation. Laser activation lasted 60 s, delivering energy densities of 17.26 J/cm² (660 nm) and 33.16 J/cm² (808 nm). S100A8/A9 levels were quantified via enzyme-linked immunosorbent assay (ELISA) and analysed using fold change from baseline, Spearman non-linear correlation analysis for age effects, Fisher's exact test, and Kruskal-Wallis tests (α = 0.05). There was inter‑individual variation in baseline S100A8/A9 levels in both PB and GCF. Baseline S100A8/A9 levels were higher in GCF than in PB at the individual level, with no age effect in PB, whereas GCF levels were lower in the 60-80‑year group than in the 45-59‑year group. PBM at 660 nm and 808 nm produced numerically greater fold increases in S100A8/A9 in PB and GCF than sham, particularly for 660 nm in older participants, but these effects did not reach the threshold for statistical significance. This study is the first clinical trial to explore the effect of S100A8/A9 expression in PB and GCF following a single PBM treatment at wavelengths of 660 nm and 808 nm. This pilot study demonstrated that S100A8/A9 can be detected in pulp blood and GCF from patients with SIP and may serve as a potential biomarker for PBM response, although no statistically significant differences were found. Given the cumulative and time-dependent nature of PBM effects, future research should investigate multi-dose protocols to better define its role in managing pulpal inflammation. - Source: PubMed
Publication date: 2026/08/29
Zhu MeifangRanjit ElizaSilva Figueredo Carlos MarceloWalsh Laurence JamesGeorge Roy - Myeloid differentiation primary-response protein 88 (MyD88), an adapter protein used by many Toll-like receptors (TLRs), plays a critical role in initiating inflammatory responses. Our laboratory has previously shown that alcohol intoxication combined with burn injury causes intestinal tissue damage and leakiness. This is accompanied by increased intestinal neutrophil infiltration along with bacterial abundance and translocation. An overgrowth of bacteria can activate TLRs on intestinal epithelial cells (IECs), promoting inflammation and subsequent gut tissue damage. To examine the role of MyD88 in intestine inflammation/leakiness following ethanol and burn injury, we used MyD88-/- mice. MyD88 deficiency in mice prevented the increases in IL-6 and KC levels, MPO activity, as well as the expression of neutrophil mediators Lipocalin2, S100a8, and S100a9 in the intestine. It also attenuated neutrophil extracellular trap (NET) formation and release of superoxide anion (O2-). In addition, MyD88 deficiency improved tight junction; namely ZO-1, Occludin, Claudin 4 and Claudin 8 expression. Finally, using IEC specific MyD88-/-IEC mice, we further found that MyD88 deficiency mitigated intestinal permeability in ethanol and burn. Together, these findings suggest that MyD88 plays a critical role in intestinal inflammation and barrier leakiness following ethanol and burn injury, and therefore, targeting the MyD88 pathway may have therapeutic potential for intervention in burn injury. - Source: PubMed
Publication date: 2026/08/29
Li XiaolingMurray Mary GraceLuck Marisa EAkhtar SuhailCannon Abigail RChoudhry Mashkoor A - Ulcerative colitis (UC) is a chronic inflammatory disease that seriously endangers human health. Shaoyao Decoction (SYD) has been widely used in clinical practice to treat UC; however, its active components and molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/08/20
Cui HuantianPei HuanMin FeitianWang YumingLong YuanChen XiaChen LifangZhou XiaonaXing LiweiWen WeiboLi YalinBian YuhongWang Ning