Rabbit S100A9 Polyclonal Ab
- Known as:
- Rabbit S100A9 Polyclonal Antibody
- Catalog number:
- 61-0189-5
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Rabbit S100A9 Polyclonal
Related genes to: Rabbit S100A9 Polyclonal Ab
- 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
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- Suxiao Jiuxin Pills (SJP), as a classic Chinese patent medicine formula, is clinically used to treat angina pectoris and myocardial ischemia (MI). However, its pharmacodynamic basis and potential molecular mechanisms remain incompletely elucidated. Bioinformatics analysis identified S100A9 as a key MI target, and ligustilide (Lig) (primary active component of SJP) as its specific ligand. - Source: PubMed
Publication date: 2026/05/18
Guo YingLi MengyaoFang ZhiruiLiu TingWang TianyuZhi HuiChen PingWang ShaoxiaChen LuSun WangjieLiu QiWang Hong - This study aimed to evaluate salivary cotinine and S100A8/A9 levels in children exposed to ETS and to examine the relationship between exposure intensity and inflammatory biomarker expression. - Source: PubMed
Publication date: 2026/05/15
Kockanat ArzuAcipinar Sukran - The window of implantation is a critical period for embryo implantation. Ovarian stimulation can disrupt endometrial receptivity, potentially through altered gene expression and downstream protein profiles. However, the impact on the endometrial proteome remains underexplored. Identifying biomarkers of endometrial receptivity may provide an opportunity to develop targeted interventions aimed at improving implantation outcomes. This prospective, case-crossover, open-label study was conducted at the Department of Human Reproduction, Division of Obstetrics and Gynecology, University Medical Centre Ljubljana, Slovenia, from September 2023 to June 2024. The study included 15 women aged <43 years with primary infertility and poor ovarian response. Endometrial samples were collected using a pipelle biopsy during the window of implantation in spontaneous and stimulated cycles and analyzed using protein microarrays targeting 1,466 proteins. Differential protein abundance was assessed using a multi-factorial linear model, including patient-specific effects as an additional factor to account for the paired case-crossover design. Effect sizes are reported as log2-fold changes with corresponding 95% confidence intervals. Differential abundance was defined a priori as |log2FC| > 0.5 with FDR-adjusted p-value < 0.05. Comparison of endometrial samples from spontaneous and stimulated cycles revealed 114 antibodies with differential abundance. Key proteins were associated with immune response (IL-8, proteins S100-A8 and S100-A9, CAMP) and extracellular matrix remodeling (MMP-9). Exploratory KEGG pathway mapping suggested involvement of immune and inflammatory pathways, including cytokine-cytokine receptor interaction and IL-17 signaling. Cluster analysis demonstrated distinct proteomic patterns, with all stimulated-cycle samples showing alterations and a subset of stimulated-cycle samples (40%) exhibiting more pronounced changes. The findings indicate that ovarian stimulation is associated with measurable alterations in the endometrial proteomic profile during the window of implantation. These changes may be relevant to biological pathways involved in endometrial receptivity and implantation. Further studies in larger cohorts are needed to validate the identified candidate markers and determine their clinical relevance for implantation outcomes. Trial registration: ClinicalTrials.gov NCT06804174. - Source: PubMed
Publication date: 2026/05/19
Abdulkhalikova DzhamilyatBan Frangež HelenaBurnik Papler TanjaŠtimpfel MartinVrtačnik Bokal EdaŠalamun Vesna - Traumatic brain injury (TBI) frequently leads to severe systemic complications, with pulmonary dysfunction acting as a major determinant of poor prognosis in survivors. While the lung microbiota is increasingly recognized as a critical regulator of pulmonary immune homeostasis, the specific mechanisms by which TBI remotely remodels the lung microenvironment to exacerbate secondary insults, such as sepsis-induced acute lung injury (ALI), remain poorly understood. To investigate this mechanism, we established a murine model combining controlled cortical impact with LPS-induced sepsis and analyzed bronchoalveolar lavage fluid by 16S rRNA sequencing and untargeted metabolomics. We further conducted microbiota depletion and transplantation experiments to establish causality, alongside molecular docking, Co-IP (co-immunoprecipitation), and transgenic mouse models to elucidate molecular pathways. Our results demonstrate that TBI significantly disrupts the lung microbiota, characterized by a reduction in Corynebacterium, and decreases the levels of the metabolite deoxyinosine. Microbiota transplantation from TBI mice worsened sepsis-induced lung injury in recipients, whereas deoxyinosine administration alleviated tissue damage by promoting the polarization of alveolar macrophages from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype. Mechanistically, deoxyinosine binds directly to S100A9, competitively inhibiting its interaction with the Receptor for Advanced Glycation End Products (RAGE), which subsequently suppresses downstream NF-κB signaling. This study identifies a novel brain-lung axis interaction mediated by microbiota-derived deoxyinosine and highlights the S100A9/RAGE pathway as a promising therapeutic target for preventing post-TBI multi-organ dysfunction. - Source: PubMed
Publication date: 2026/05/18
Wang BailunGu AngranYang YizhengLiu XuanLiu RunmengWang Yuelan - Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) represent a critical subset of immunosuppressive cells within the tumor microenvironment. Their interaction with breast cancer stem cells (BCSCs) constitutes a vital link that drives the malignant progression of breast cancer, particularly in triple-negative breast cancer (TNBC). However, the precise molecular mechanisms through which these cells mediate BCSC-related stemness reprogramming and enhanced metastatic potential in breast cancer remain inadequately understood. In this study, PMN-MDSCs were isolated from mouse breast cancer solid tumor tissues. Functional characterization was conducted using flow cytometric phenotyping, nuclear morphology analysis, and T cell immunosuppressive function assays. In vivo tumorigenesis experiments confirmed their pro-tumor growth effects and enhanced tumor stem cell characteristics. Concurrently, the CD44CD24 subpopulation of 4T1 cells was sorted to systematically verify their tumor stem cell properties and stemness plasticity. In vitro co-culture experiments demonstrated that PMN-MDSCs significantly increased the proportion of CD44CD24 stem-like subpopulations in 4T1 cells, prompting non-stem cells to differentiate into stem cell-like cells. They also promoted STAT3 phosphorylation, upregulated the expression of stemness-related proteins and mesenchymal markers, downregulated the epithelial marker E-cadherin, and markedly enhanced CXCL5 secretion. These effects were effectively reversed by the stemness inhibitor Napabucasin. Transwell non-contact co-culture and exosome function assays further confirmed that PMN-MDSCs regulate cancer cell stemness in a paracrine manner. S100A9, a key effector molecule in their exosomes, induced CXCL5 secretion by activating the STAT3 pathway. CXCL5 subsequently activated both the ERK1/2 and STAT3 pathways through autocrine and paracrine mechanisms, enhancing tumor cell metastatic potential and establishing a positive feedback loop that sustains its own secretion. This loop effect was blocked by a CXCL5-neutralizing antibody. Single-cell sequencing data analysis and clinical sample validation of TNBC indicated significantly elevated infiltration of myeloid cells, as well as increased S100A9 and CXCL5 expression levels in cancer tissues, alongside a marked upregulation of the mRNA stemness index. The stemness index was closely associated with poor patient prognosis. In summary, this study reveals that PMN-MDSCs can activate the STAT3-CXCL5-ERK positive feedback regulatory axis via exosomal S100A9, synergistically enhancing breast cancer cell stemness and metastatic capacity. These findings provide a theoretical reference and potential intervention targets for targeting the tumor microenvironment to inhibit TNBC progression. - Source: PubMed
Publication date: 2026/05/18
Wang BoSu BinjieCai QiJiang TaoLiu WeidongZhao XiaoguoXu YuekangGuo ChangyingLi Jinyao