S100A9 _ Calgranulin_B _ MRP14
- Known as:
- S100A9 _ Calgranulin_B _ MRP14
- Catalog number:
- BM4027X
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- S100A9 _ Calgranulin_B MRP14
Related genes to: S100A9 _ Calgranulin_B _ MRP14
- 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 _ Calgranulin_B _ MRP14
Related articles to: S100A9 _ Calgranulin_B _ MRP14
- Type 1 diabetes mellitus (T1DM) compromises the mechanical adaptive capacity of bones, posing challenges in orthodontic treatment and increases periodontal complication risks. Mechanical loading is the main inducer of craniofacial bone adaptation; however, the early proteomic responses of the maxillary bone to stress under diabetic conditions remain unexplored. Therefore, we aimed to characterize the early proteomic signatures of the maxillary bone in T1DM rats subjected to controlled mechanical stress and identify potentially relevant molecular pathways for orthodontic treatment in patients with diabetes. - Source: PubMed
Publication date: 2026/04/06
Tobias-López Luis FernandoTrejo-Iriarte Cynthia GeorginaGarcía-Muñoz AlejandroGómez-Clavel José Francisco - Radiation-induced heart disease (RIHD) is a serious complication of thoracic radiotherapy, and its pathogenesis involves systemic immune alterations. To elucidate these mechanisms, we profiled peripheral blood mononuclear cells (PBMCs) from patients before and after thoracic radiotherapy using single-cell RNA sequencing (scRNA-seq), with key findings validated via multiparameter flow cytometry and ELISA assays. Our analysis revealed that radiotherapy markedly reshaped the immune composition, expanding innate myeloid cells (monocytes and neutrophils) and reducing lymphocytes (T and NK cells); these compositional shifts were independently confirmed by flow cytometric analysis. Cell-cell communication networks showed that postradiotherapy monocytes evolved into central signaling hubs, exhibiting heightened proinflammatory ligand-receptor interactions. Consistent with this, monocytes showed broad transcriptional reprogramming with upregulation of canonical inflammatory pathways (IL-6/STAT3, TNF/NF-κB) and metabolic regulators (mTORC1, glycolysis). ELISA assays corroborated these transcriptomic signatures, demonstrating significantly elevated plasma levels of IL-6 and TNF-α post-treatment. Notably, scRNA-seq identified a selective expansion of the highly plastic intermediate (CD14++CD16+) monocyte subset, a specific population shift further verified by flow cytometry. These intermediate monocytes exhibited an immature, progenitor-like profile and were enriched at the origin of a Monocle3 pseudotime trajectory. Trajectory analysis indicated they differentiate into mature classical monocytes that upregulate proinflammatory effector genes such as S100A8, S100A9, and S100A12. Furthermore, pseudotime gene clustering revealed a functional bifurcation in monocyte behavior: one module drove inflammatory activation, while a second module simultaneously engaged oxidative stress responses and antioxidant defenses (e.g., glutathione metabolism). In summary, by integrating single-cell transcriptomics with experimental validation, we demonstrate that radiotherapy drives a systemic immune shift characterized by intermediate monocyte expansion and bifurcated programs of inflammation and stress adaptation. Intermediate monocytes emerge as key drivers of postradiotherapy inflammation, offering a potential cellular biomarker of RIHD risk and a target for immunomodulatory interventions to mitigate cardiovascular injury in cancer survivors. - Source: PubMed
Publication date: 2026/04/17
He JinchenKong DejunZhang ChengweiChen QiuhongYang HongWang YuyuanWu TianqiWu Qi - Oxidative stress (OS) plays a role in hypertension development, but the underlying genetic mechanisms are not completely understood. This study aimed to investigate the association between OS-related genes and hypertension by performing an integrative multi-omics analysis using summary-data-based Mendelian randomization (SMR) and colocalization approaches. - Source: PubMed
Publication date: 2026/03/25
Zhang YueMeng JinyangYan YuchengTang HongZhong DonglingLi YuxiXue PeiwenZhang AnrenJin RongjiangLi Juan - Atopic dermatitis (AD) is a common chronic inflammatory skin condition affecting humans and animals, including dogs. The underlying mechanisms in both species are intricate and varied, yet they demonstrate notable similarities. Although numerous transcriptome profiles have been analyzed separately for each species, comparative studies are relatively scarce. We performed a meta-analysis of gene expression datasets from the affected skin of dogs and humans. Enrichment analysis of commonly shared differentially expressed genes (DEGs) derived from two canine datasets revealed an IL-27-mediated signaling pathway. Furthermore, after examining two published GEO datasets from humans and two from canines, we identified fifteen conserved DEGs across all datasets (p < 0.05). The enrichment assessment of the upregulated genes indicated that S100A8 and S100A9 are associated with the Th17 signaling pathway, while FHL1 and STAT1 are linked to JAK-STAT signaling pathways. CCL13, identified as a Th2-related chemokine, displayed increased expression in both canine and human AD. Consequently, these proteins may serve as potential biomarkers and therapeutic targets for AD in both species. Additionally, three gene products-HSD11B1, IL-34, and NELL2-showed different expression patterns in humans and dogs with AD, suggesting that specific genes may have distinct roles in the pathogenesis of AD across species. - Source: PubMed
Publication date: 2026/04/16
Wang YuRichmond Jillian MAlmela Ramon M - Renal interstitial fibrosis is a key pathological feature associated with the progression of chronic kidney disease (CKD) progression. Macrophages play a central role in renal inflammation and fibrosis, and the S100 calcium binding protein A8/A9 (S100A8/A9) protein that they express participates in the immune response as an important regulatory inflammatory factor. Therefore, this study aimed to investigate the role of S100A8/A9 in M2-driven macrophage-to-myofibroblast transition (MMT) during progressive fibrosis in patients with CKD. We analyzed renal biopsy tissues from patients with CKD, constructed S100A9 overexpression and macrophage-specific knockdown mouse models, and developed an in vitro transforming growth factor β1 (TGF-β1)-induced MMT cell model. Our results revealed that S100A8/A9 was significantly upregulated in fibrotic kidneys and was mainly expressed in CD68/F4/80 macrophages with an MMT phenotype. Further experiments demonstrated that S100A9 knockdown significantly reduced renal interstitial fibrosis, collagen deposition, and tissue damage in mice with unilateral ureteral obstruction (UUO), and inhibited MMT. Conversely, S100A9 overexpression exacerbated the fibrotic phenotype. Moreover, both in vitro and in vivo, knockdown of S100A9 or pharmacological inhibition with the S100A8/A9 inhibitor paquinimod blocked the activation of the toll-like receptor 4 (TLR4)/ myeloid differentiation primary response gene 88 (MyD88)/ nuclear factor kappa-B (NF-κB) signaling pathway, reduced M2 macrophage polarization, and attenuated MMT. These findings suggest that S100A8/A9 may drives M2 macrophage-mediated MMT via the TLR4/NF-κB pathway, thereby promoting renal fibrosis. Therefore, targeting S100A8/A9 may represent a promising approach for the treatment of renal fibrosis in CKD. - Source: PubMed
Publication date: 2026/04/16
Chen XulongZha WeiweiShen JiangwenLi LinFu YanfangTian PuXunZheng BingxuanLi Cheng