S100A9 _ Calgranulin_B _ MRP14
- Known as:
- S100A9 _ Calgranulin_B _ MRP14
- Catalog number:
- NBP1-40751
- Product Quantity:
- 0.1 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
- Primary open-angle glaucoma (POAG) is a progressive optic neuropathy that leads to irreversible vision loss, primarily due to dysfunction of the trabecular meshwork (TM). Although impaired autophagy has been implicated in POAG pathogenesis, its molecular drivers remain poorly defined. This study systematically investigated autophagy-related genes (ATGs) in TM tissue from POAG patients. Transcriptomic datasets (GSE4316 and GSE27276) were analyzed to identify differentially expressed genes (DEGs). A curated list of autophagy-related genes (ATGs) from HADb and GeneCards was intersected with DEGs to identify differentially expressed ATGs (DEATGs). Functional analyses included Gene Ontology (GO) and KEGG pathway enrichment, protein-protein interaction (PPI) network construction, hub gene identification, immune cell infiltration profiling via single-sample gene set enrichment analysis (ssGSEA), and molecular docking to evaluate predicted interactions between latanoprost and hub proteins. A total of 990 DEGs were identified, including 15 DEATGs. Among these, S100A8 and S100A9 emerged as hub genes, exhibiting strong functional similarity and central roles within the PPI network. Enrichment analysis revealed significant involvement in autophagy regulation, tyrosine metabolism, and oxidative phosphorylation. Notably, molecular docking predicted high-affinity binding between latanoprost and S100A9. Immune profiling demonstrated significant alterations in both innate and adaptive immune cell populations, including a strong positive correlation between S100A9 expression and Th2 cell abundance. These findings suggest that S100A9 may act as a central regulator linking autophagy deficiency to immune dysregulation in POAG. Its predicted interaction with latanoprost highlights a potential molecular mechanism for pharmacologic modulation of TM homeostasis, supporting the therapeutic value of targeting S100A9-mediated autophagy-immune crosstalk in intraocular pressure control. - Source: PubMed
Publication date: 2026/03/11
Hu LiliPan ShaoxinChen GongLei MinAi MingLv XiangyunPan HaoningWang PengChang Rui - The most common ocular neoplasia among children is retinoblastoma. Currently, the diagnosis of this disease is essentially clinical, taking a biopsy is contraindicated owing to the high risk of causing metastasis. Therefore, it is imperative the development of a method to diagnose this disease through a non-invasive fashion. We choose tears as they fulfill the former precept. Through proteomic analysis we observed 52 up regulated and 48 down regulated proteins among retinoblastoma cases as compared to healthy children. Among these proteins, we identified several previously associated with retinoblastoma such as apolipoprotein A-1 (). We confirmed up regulation of and S100 binding calcium A9 () which revealed faithful concordance to the predicted values from mass spectrometry. - Source: PubMed
Publication date: 2026/04/22
Rodríguez-Rodríguez AndrésCalderón-González Karla GriselLuna-Arias Juan PedroMoctezuma-Dávila MarianaRangel-Charqueño MarthaYañez-Soto BernardoOlivares-Illana VanesaHernández-Monge Jesús - Immunotherapy has emerged as a promising strategy for multiple myeloma (MM), yet relapse remains frequent due to the immunosuppressive bone marrow (BM) microenvironment, characterized by T cell dysfunction and accumulation of immunosuppressive myeloid cells. The co-stimulatory receptor 4-1BB (CD137, TNFRSF9) can enhance T and NK cell effector functions, but its therapeutic utility in MM is not well established. Tasquinimod (TQ), a clinical-stage S100A9 inhibitor, offers a complementary approach by limiting the recruitment and activity of suppressive myeloid cells. - Source: PubMed
Publication date: 2026/05/04
Satilmis HaticeDenis AdrienVerheye EmmaVan der Vreken ArneZhan DewenCalliauw EvanTörngren MarieEriksson HelenaFaict SylviaDe Bruyne ElkeMenu ElineVanderkerken KarinDe Veirman Kim - Fibrosis is a progressive and irreversible mechanism affecting any organ. During tissue injury, fibroblast activation is necessary for wound healing but the uncontrolled accumulation of fibrotic tissue leads to local organ damage. The fibrotic process involves the excessive accumulation of extracellular matrix components and inflammatory mediators. Since sustained inflammation precedes fibrosis, the involvement of immune cells, like neutrophils, monocytes and macrophages, is crucial to elucidate its pathogenesis. These immune cells release proinflammatory cytokines and chemokines, and also proteins that act as fibroblast proliferation mediators, such as the S100/calgranulins subgroup, comprising S100A8, S100A9, and S100A12 proteins. Moreover, a homodimer of S100A8 binds to a homodimer of S100A9 forming the heterodimer S100A8/A9, called calprotectin, which is abundant in the cytosol of neutrophils during immune activation. Although calprotectin (S100A8/A9) is the most predominant form, calgranulins S100A8 and S100A9 have independent functions of calprotectin (S100A8/9) complex formation. These calcium-binding proteins have proinflammatory functions and are potential inflammation biomarkers. More evidence in different fibrosis disorders highlights their role as relevant fibroblast proliferation mediators and prognosis markers. Hence, this review focuses on the current understanding of the role of S100A8, S100A9, and S100A12 calgranulins and calprotectin (S100A8/A9) in the fibrotic process of different disorders, and their potential application as disease severity and prognosis biomarkers. - Source: PubMed
Publication date: 2026/04/09
Regino-Zamarripa Nora ElemiBurciaga Ana SofíaBocanegra-Mondragón MoisésCruz-Lagunas AlfredoCamarena ÁngelJiménez-Alvarez LuisRamírez RemediosRamírez-Martínez GustavoZúñiga Joaquín - Cancer-associated cachexia (CAC) is a multifactorial wasting syndrome characterized by progressive loss of fat and lean mass, systemic inflammation, and poor therapeutic responsiveness. While brown adipose tissue (BAT) is traditionally considered a protective, energy-dissipating organ, its qualitative remodeling in CAC remains poorly characterized.Here, we demonstrate that CAC induces a senescent conversion of BAT, marked by thermogenic failure, fibrosis, inflammation, and acquisition of a senescence-associated secretory phenotype (SASP). Through integrative transcriptomic, proteomic, and secretomic analyses in a murine model of lung cancer-induced cachexia, we identify S100A9 as a key factor selectively upregulated and secreted by brown adipocytes. Functional assays reveal that the BAT secretome exerts deleterious paracrine effects on white adipocytes and skeletal myotubes, promoting lipolysis and atrophy, while also impairing brown adipocyte identity in an autocrine manner. Co-culture and gain-of-function experiments with S100A9 recapitulate these phenotypes in vitro in mouse and human brown adipocytes, whereas pharmacological blockade of S100A9 signaling partially restores thermogenic and metabolic features. Collectively, our findings reveal that BAT undergoes functional reprogramming into a senescent and secretory tissue in cancer cachexia, with adipocyte-derived S100A9 acting as a novel pro-cachectic mediator. This work redefines the role of BAT in CAC and identifies S100A9 as a potential therapeutic target within the adipose-muscle crosstalk. - Source: PubMed
Publication date: 2026/05/02
Di Biagio ClaudiaTortolici FlaviaGaudioso FrancescoNinni AndreaGiurdanella Annina FrancescaDe Ranieri ChiaraZaccaria FabioSciarretta FrancescaLuca VerteramoArciprete FrancescaCarotti SimoneAf de Vries AntoineKooijman SanderPacello FrancescaBattistoni AndreaLettieri-Barbato DanieleAquilano Katia