ANXA1 antibody - N-terminal region (ARP36569_P050)
- Known as:
- ANXA1 (anti-) - N-terminal region (ARP36569_P050)
- Catalog number:
- arp36569_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ANXA1 antibody - N-terminal region (ARP36569_P050)
Related genes to: ANXA1 antibody - N-terminal region (ARP36569_P050)
- Gene:
- ANXA1 NIH gene
- Name:
- annexin A1
- Previous symbol:
- ANX1, LPC1
- Synonyms:
- -
- Chromosome:
- 9q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: ANXA1 antibody - N-terminal region (ARP36569_P050)
Related articles to: ANXA1 antibody - N-terminal region (ARP36569_P050)
- Impaired macrophage efferocytosis is a major barrier to timely inflammatory resolution in chronic diabetic wounds. We developed an aligned core-shell gelatin/chitosan dressing for local delivery of losmapimod, a p38 MAPK inhibitor, and achieved a controlled, time-decreasing release profile while preserving wet-state structural integrity. In vitro, losmapimod upregulated ANXA1 and enhanced both macrophage efferocytosis and phagocytic activity. In db/db wounds, the losmapimod-loaded scaffold accelerated healing and improved multiple histological features of pro-healing remodeling, including reduced fibrotic signaling, enhanced vascularization, increased epithelial progenitor-associated signals, and more mature collagen organization. Transcriptomic analysis further supported attenuation of inflammatory recruitment-associated programs together with enrichment of epidermal repair-related pathways. Gain- and loss-of-function studies in macrophages, together with in vivo pharmacological modulation, implicated ANXA1-related signaling as an important contributor to these effects. Together, these findings support a local, time-programmed pro-resolution biomaterial strategy for diabetic wound repair and identify macrophage clearance-associated remodeling as a relevant therapeutic axis. - Source: PubMed
Publication date: 2026/05/29
Yang XiLi BolinLi WeiWang ZiruiZhao KexuanHu ZhonghaoPeng YahanYang TongtongWang Chenbing - Clinically actionable biomarkers that reliably distinguish glioblastoma (GBM) from lower-grade glioma (LGG) across expression platforms remain an unmet need. Existing transcriptomic signatures are frequently confounded by batch effects, platform heterogeneity, and the inability to translate to single-patient clinical workflows. We developed a topology-aware biomarker discovery framework in which analysis-of-variance ranking defines a candidate gene pool, hypergraph co-expression analysis at correlation threshold = 0.75 identifies densely connected hubs within this pool, rough set reduct optimisation selects a minimal sufficient subset of these hubs, and a Random Forest classifier with stratified cross-validation performs the final discrimination. The pipeline was trained exclusively on GSE16011, a single-platform single-institution Affymetrix microarray cohort free from batch-class confound, and validated on two independent RNA-sequencing cohorts (CGGA-325 and CGGA-693). Robustness was further assessed through bootstrap optimism correction, DeLong cross-cohort equivalence testing, leave-one-gene-out analysis, and a sensitivity analysis under WHO CNS5 (2021) class definitions. The pipeline identified a ten-gene biomarker panel (, , , , , , , , , and ), achieving a fivefold cross-validation AUROC of 0.906 ± 0.029 and a held-out AUROC of 0.831. External validation yielded AUROC = 0.838 in CGGA-325 and AUROC = 0.836 in CGGA-693. The biomarker-derived risk score demonstrated independent prognostic value in CGGA-693 (multivariate Cox hazard ratio = 9.195; < 0.001) after adjustment for WHO histological grade, with Kaplan-Meier analysis confirming highly significant survival separation (log-rank = 4.60 × 10). Class definitions in the present work follow the histology-based pre-2021 WHO classification used in the source datasets and do not directly incorporate WHO CNS5 (2021) molecular criteria, such as IDH mutation status, that distinguish IDH-wild-type glioblastoma from IDH-mutant grade-IV astrocytoma. After excluding IDH-mutant grade-IV cases from the CGGA cohorts, the classification AUROCs increased to 0.906 in CGGA-325 and 0.872 in CGGA-693, with a Cox risk-score hazard ratio of 8.57 ( = 1.4 × 10) and log-rank = 1.4 × 10 retained on the CNS5-aligned cohort. The methodological contributions introduced in this study, namely, the topology-aware hypergraph candidate pool construction, the rough set combinatorial reduct selection, the fixed-reference single-sample normalisation protocol, and the nested validation regime combining bootstrap optimism correction with cross-platform DeLong testing, are platform agnostic and directly applicable to future CNS5-aligned cohorts as such resources become publicly available, supporting the prospective re-derivation of molecularly defined glioma signatures within the integrated histopathological and molecular frameworks of contemporary neuro-oncology. - Source: PubMed
Publication date: 2026/05/12
Akgüller ÖmerBalcı Mehmet AliCioca Gabriela - Although the extracellular matrix (ECM) is a highly dynamic partner of the immune system, its immunoregulatory role during the early phase of sepsis-induced acute lung injury (ALI) remains poorly defined. Using a murine cecal ligation and puncture (CLP) model, we observed dynamic ECM remodeling characterized by rapid collagen loss within 24 h, followed by a pathological fibroproliferation phase. Proteomic profiling of the degraded ECM demonstrated its immunoregulatory potential. In vitro studies revealed that annexin A1 (ANXA1), an upregulated ECM component, promoted anti-inflammatory macrophage polarization via the formyl-peptide receptor 2/lipoxin A4 (FPR2/ALX)-dependent 5'-adenosine monophosphate-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway. However, under pathological conditions, collagen loss markedly reduces the number of key binding sites for integrin β1 (Itgb1), thereby disrupting macrophage-ECM adhesion and resulting in macrophage detachment; upon entering the inflammatory microenvironment, these cells acquire a proinflammatory phenotype, exacerbating pulmonary inflammation. Capitalizing on the collagen biosynthetic function of ascorbic acid (AA), we investigated its capacity to restore macrophage-ECM adhesion therapeutically. In vitro, treatment of fibroblasts with AA on decellularized CLP-ECM increased collagen deposition and improved macrophage adhesion. In vivo, intratracheal instillation of AA (20 mg/kg) enhanced collagen biosynthesis, which promoted ECM restoration, sustained interstitial macrophage retention, suppressed proinflammatory cytokine production, and ultimately resolved lung injury. Our study reveals that ECM degradation is an early immunoregulatory event and suggests a therapeutic approach for ECM repair via airway-targeted AA delivery in ALI. - Source: PubMed
Publication date: 2026/05/22
Xie FeiyanSun YuhengWei XinyanZhang WeiLuo WeiHuang JieFang ShencunZhang XinxinQiu HaiboChao Jie - Annexin A1 (AnxA1) is a key anti-inflammatory mediator that regulates both innate and adaptive immunity, promoting resolution of inflammation and tissue repair. It is highly expressed in neutrophils, macrophages, dendritic cells, and select lymphocyte subsets, where it limits excessive immune activation and maintains immune homeostasis. Through binding to the G protein-coupled receptor formyl peptide receptor 2 (FPR2/ALX), AnxA1 induces neutrophil apoptosis and promotes macrophage polarization toward an anti-inflammatory M2 phenotype. In adaptive immunity, AnxA1 regulates CD4 T-cell differentiation in a lineage-specific manner, promoting Th1 and Th17 responses while suppressing Th2 polarization; its deficiency skews T cells toward a Th2 phenotype with increased IL-4/IL-13 and reduced IL-17, highlighting its role in maintaining T-cell balance. In autoimmune and inflammatory disorders such as rheumatoid arthritis, lupus, type-1 diabetes, and multiple sclerosis, hyperactivation of toll-like receptor-4 (TLR4) and epidermal growth factor receptor (EGFR) drives STAT1-dependent signaling, sustaining cytokine production and tissue injury. The Annexin A2 (AnxA2)-EGFR complex further amplifies this response by downregulating AnxA1 and reinforcing pro-inflammatory signaling pathways. In contrast, AnxA1 engagement with EGFR and FPR2 redirects signaling toward STAT3, enhancing IL-10 and TGF-β production while suppressing STAT1-driven pathways. This STAT1-STAT3 balance is critical for immune resolution, inflammation control, and tissue homeostasis. Therapeutically, AnxA1-based strategies suppress STAT1 signaling and promote a regulated STAT3/SOCS3 axis associated with immune resolution, while limiting pathogenic Th17-associated STAT3 activity. Overall, AnxA1 acts as a molecular switch integrating receptor-mediated signals to fine-tune immune responses and mitigate tissue damage in chronic inflammatory and autoimmune diseases. - Source: PubMed
Publication date: 2026/05/19
Ambrish ThrupthiJayaswamy Pavan KHaridas VikramKellarai AdithiShetty SukanyaShetty Praveenkumar - Necrotizing enterocolitis (NEC) is a severe neonatal intestinal disease with high mortality, and effective pharmacological therapies remain limited. Increasing evidence suggests that multiple forms of programmed cell death are involved in NEC pathogenesis. Glutathione (GSH), has shown potential protective effects against oxidative stress and inflammation injury, but its role and underlying mechanisms in NEC remain unclear. This study aimed to elucidate the shared molecular mechanisms underlying ferroptosis, pyroptosis, necroptosis and autophagy in NEC, and to investigate the protective role and regulatory pathways of GSH against these forms of programmed cell death. - Source: PubMed
Publication date: 2026/03/25
Zou PengjianHe QiumingHou LonglongLi LinHuang YaqiLuo WenjieWang JunjieYan BinLin ZefengTang WenfengLv JunjianWang ZheYu JiakangLiu JiaoXia HuiminZhong Wei