S100A9 antibody Monoclonal Antibodies Primary antibodies
- Known as:
- S100A9 (anti-) Monoclonal Antibodies Primary antibodies
- Catalog number:
- orb43047
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- S100A9 antibody Monoclonal Antibodies Primary antibodies
Related genes to: S100A9 antibody Monoclonal Antibodies Primary antibodies
- 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 antibody Monoclonal Antibodies Primary antibodies
Related articles to: S100A9 antibody Monoclonal Antibodies Primary antibodies
- Standardized molecular methods to assess the host response to breast implants are lacking. Mass spectrometry-based proteomics offers an unbiased approach to characterize the capsule proteome and the foreign-body response. - Source: PubMed
Publication date: 2026/09/10
Larsen AndreasØstergaard OleWeltz Tim KongsmarkTran John Vinh QuangBak Erik Eiler FrydshouGuðjónsdóttir Linda RegínaHemmingsen Mathilde NejrupØrholt MathiasVester-Glowinski PeterWoetmann AndersOlsen Jesper VelgaardHerly Mikkel - S100A8 and S100A9 are critical members of the S100 protein family with diverse immunoregulatory functions, serving as important mediators of neuroimmune communication and key links between inflammation, microglial activation, and neurodegenerative processes. S100A8 and S100A9 are abundantly expressed in neutrophils, monocytes, and other immune cells and are rapidly released during inflammatory responses. Once extracellular, S100A8/A9 interacts with cell-surface pattern-recognition receptors, including TLR4 and RAGE, triggering downstream NF-κB and MAPK signaling cascades that drive pro-inflammatory cytokine production. S100A8/A9 has also been implicated in activating the intracellular NLRP3 inflammasome sensor/scaffold, a pro-inflammatory response associated with neuroinflammation. Growing evidence indicates that dysregulated S100A8/A9 expression contributes to both central and peripheral inflammatory pathologies and is elevated across multiple disease states. This review provides a comprehensive analysis of the S100A8/A9 signaling axis, examining its structural and functional roles in regulating microglial activation and neuroimmune crosstalk. It further explores the role of S100A8/A9 signaling in the pathogenesis of diverse inflammatory and neurodegenerative disorders, highlighting the underlying molecular mechanisms. By integrating current knowledge, this review highlights the therapeutic potential of targeting the S100A8/A9 to modulate neuroinflammation and facilitate the development of more effective interventions for neurodegenerative diseases. - Source: PubMed
Publication date: 2026/08/24
Malik Jonaid AhmadQamar ToobaQadri Abrar HFaheem Iqball - Periprosthetic joint infection (PJI) is a debilitating and dangerous complication following joint arthroplasty procedures. With the increasing incidence of arthroplasty procedures, the burden of PJI is expected to continually grow. A correct and early diagnosis of PJI proves difficult, with the lack of a single standardized molecular test. The utilization of serology-based biomarkers would provide a non-invasive sampling method; however, these methods have not proven sufficient to satisfy the diagnostic criteria. - Source: PubMed
Publication date: 2026/09/04
Andree Sebastian LMorsø Linnea SalbøgSkallerup JacobLarsen-Ledet BoSøborg Mathilde VSatriano LetiziaBay-Jensen Anne CRasmussen StenThudium Christian FStensballe Allan - 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