S100A9 _ Calgranulin_B _ MRP14
- Known as:
- S100A9 _ Calgranulin_B _ MRP14
- Catalog number:
- NB600-721
- 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
- Chronic obstructive pulmonary disease (COPD) lacks reliable molecular biomarkers for early diagnosis and risk stratification beyond conventional spirometry-based assessment. Synthetic lethality (SL)-related gene prioritization provides a biologically informed framework for identifying disease-associated candidate biomarkers in COPD. In this study, we integrated public transcriptomic datasets, SL-related gene sets, and machine learning approaches to identify a diagnostic signature for COPD. Using GSE47460 as the training cohort (220 COPD and 108 controls) and GSE57148 as the external validation cohort (98 COPD and 91 controls), we identified 74 SL-related differentially expressed genes enriched in inflammatory signaling and extracellular matrix organization. LASSO regression and random forest analysis yielded a five-gene diagnostic signature consisting of CYP1B1, VEGFA, RET, FGG, and S100A9. The integrated nomogram showed good diagnostic performance in the validation cohort, with an AUC of 0.8311 (95% CI: 0.7839-0.8783), outperforming individual genes and supporting its potential use as an adjunctive molecular tool for COPD diagnosis and risk assessment. Single-cell RNA sequencing, immune infiltration analysis, and preliminary in vitro experiments further supported the biological relevance of the identified genes. Overall, this study supports SL-related gene prioritization combined with multi-omic integration as a useful strategy for COPD biomarker discovery while generating testable hypotheses regarding disease-associated vulnerability pathways. - Source: PubMed
Publication date: 2026/05/02
Yang YueWang ZengruiSu XiaorongTang JiefuZhang ZhiFan XinliXu HaitaoWang LihanLuo Zhuang - Aging profoundly alters host immunity, yet how age-associated immune changes in the liver influence the growth of metastatic tumors remains incompletely understood. Liver metastasis is a major cause of cancer-related mortality, particularly in elderly patients, for whom aggressive treatments are often not feasible. This study aimed to clarify how aging reshapes the hepatic immune microenvironment and to identify age-associated host factors that influence liver metastasis growth. Tumor-naïve and tumor-bearing young and aged mice were analyzed using a syngeneic MC38 liver metastasis model. Immune cell composition in the liver was assessed by flow cytometry, and gene expression was evaluated by quantitative reverse transcription PCR (RT-qPCR). Public transcriptomic datasets were screened to identify age-associated inflammatory factors. The functional relevance of the S100A8/A9 axis was examined using the small-molecule inhibitor paquinimod. Aging was associated with a distinct baseline immune cell composition in the liver. During liver metastasis, overall growth was comparable between young and aged mice; however, metastatic lesions in aged hosts showed increased expression of multiple inflammation-related genes and prominent accumulation of Ly6G cells. In silico screening identified as one of the most highly upregulated inflammation-related genes in aged livers, which was confirmed in both tumor-naïve and metastatic liver tissues. Pharmacological modulation of the S100A8/A9 axis with paquinimod significantly reduced liver metastasis growth in aged, but not young, mice, and was accompanied by a shift in immune cell composition, including an increased representation of CD8 T cells. These findings indicate that aging is associated with a distinct hepatic immune context that shapes the inflammatory and cellular composition of the tumor microenvironment during liver metastasis. S100A9 emerges as a key age-associated, host-derived factor that is functionally relevant to the growth of liver metastases in aged hosts, supporting the S100A8/A9 axis as a context-specific therapeutic target. - Source: PubMed
Publication date: 2026/05/19
Tsuneki TakaoSaito MasafumiYamashita KimihiroAndo MasayukiYasuda KeisukeShirakami NaotoIto RyotaAdachi YukariKagiyama HirokiTachibana TakaakiImai MasakiInubushi SachikoKanayama KazukiKoma Yu-IchiroFujita MitsuguPollok Joerg-MatthiasSugita YutakaIkeda TaroKoterazawa YasufumiAoki TomoakiHarada HitoshiOtowa YasunoriUrakawa NaokiGoto HironobuHasegawa HiroshiKanaji ShingoMatsuda TakeruKakeji Yoshihiro - Epidermal growth factor (EGF) is a therapeutically important member of a family of the growth factors that activate EGF receptors, triggering several signaling pathways vital for development, homeostasis and regeneration of many organs. Previous studies have shown the ability of S100A4, a small calcium-binding protein of the S100 family, to directly affect functional activity of EGF receptors and its ligands, including EGF. However, selectivity and functional significance of EGF-S100 interactions remain unexplored. To address this, we examined specificity of EGF for twenty-one S100 proteins using surface plasmon resonance spectroscopy. The impact of the revealed interactions on EGF-induced cellular effects was assessed using cell proliferation and metabolic activity assays. S100A2/A4/A6/A11/A12/A13/A16/P and S100A8-S100A9 heterodimer bind EGF strictly in the presence of calcium with lowest estimates of the equilibrium dissociation constant ranging from 13 nM to 1.0 μM. Structural modelling indicates involvement of α-helix IV and "hinge" region of the EGF-specific S100 proteins in the EGF binding, which was confirmed for S100P by mutagenesis. The complexation of EGF with S100A2/A6/A12/A16/P exerts distinct S100-dependent effects on viability and metabolic activity of lung adenocarcinoma A549 cells. Bioinformatics analysis showed that dysregulation of EGF and the EGF-specific S100 proteins is associated with many oncological diseases, Alzheimer's and Parkinson's diseases, psoriasis, etc. Overall, specific S100 proteins have been shown to directly modulate various aspects of EGF functioning, which may be important for ensuring efficacy of the EGFR-targeted cancer therapies, as well as for use of EGF in regenerative medicine. - Source: PubMed
Publication date: 2026/05/20
Rastrygina Victoria AVologzhannikova Alisa AChaplygina Alina VBobrova Lolita AZemskova Marina YDeryusheva Evgenia ISokolov Andrey SPermyakova Maria ELitus Ekaterina AUversky Vladimir NPermyakov Eugene APermyakov Sergei E - Psoroptic mange, caused by the mite Psoroptes ovis, poses a major challenge to global livestock production, with current control strategies limited by acaricide resistance, residue issues, and environmental concerns. This underscores the need for innovative approaches targeting parasite-host interactions. While disruption of skin barrier homeostasis is recognized as a key driver in the pathogenesis of many dermatoses, its potential as a preventive target in parasitic skin diseases remains largely undefined. Herein, we investigated the role of Psoroptes ovis macrophage migration inhibitory factor (PsoMIF) in modulating the host skin barrier and evaluated its potential as a preventive target. The impact of recombinant PsoMIF (rPsoMIF) on keratinocyte barrier markers was first analyzed in vitro using HaCaT cells. Its barrier-disrupting effect was then validated in vivo in a healthy rabbit model. Finally, the prophylactic efficacy of a PsoMIF-specific antibody (PsoMIF-IgG) was assessed in a P. ovis challenge model. In vitro, rPsoMIF significantly disturbed the proliferation-differentiation balance in HaCaT cells, upregulating markers of proliferation (Ki67, K6, K5, and K14) while downregulating key terminal differentiation proteins (FLG, IVL). It also promoted the expression of inflammatory cytokines (IFN-γ, IL-4, IL-17A) and antimicrobial peptides (LL37, S100A9). In vivo, rPsoMIF injection recapitulated key pathological features of natural infestation. Crucially, PsoMIF-IgG prophylaxis in mite-challenge rabbits significantly improved clinical signs, drastically reduced mite burden and scab weight, and alleviated barrier dysfunction by ameliorating hyperplasia, modulating the proliferation-differentiation balance, and suppressing inflammation. Importantly, an in vitro acaricidal assay confirmed that PsoMIF-IgG lacks direct mite-killing activity, underscoring that its prophylactic efficacy is mediated through host-directed mechanisms. Our findings identify PsoMIF as a critical pathogenic mediator that drives skin barrier dysfunction in psoroptic mange. Targeting blockade of PsoMIF represents a novel prophylactic strategy for psoroptic mange control. - Source: PubMed
Publication date: 2026/05/21
Gu X BFan JFang C LWu F YYao X YJiPo E H ZXu JHe R - Sepsis mortality stems from infection-triggered immune dysregulation, causing multiple organ dysfunction. B cells, key to adaptive immunity, protect against infection and regulate inflammation through antibodies, cytokines, and cell signaling. Their dysfunction is linked to sepsis outcomes, but their dynamic differentiation and underlying mechanisms remain poorly understood. - Source: PubMed
Publication date: 2026/05/16
Zhuo XiumingJian GangrenChen Hongyi