ANXA2 (Phospho-Ser26) Antibody
- Known as:
- ANXA2 (Phospho-Ser26) Antibody
- Catalog number:
- 11839
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- ANXA2 (Phospho-Ser26) Antibody
Related genes to: ANXA2 (Phospho-Ser26) Antibody
- Gene:
- ANXA2 NIH gene
- Name:
- annexin A2
- Previous symbol:
- ANX2, ANX2L4, CAL1H, LPC2D
- Synonyms:
- LIP2
- Chromosome:
- 15q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: ANXA2 (Phospho-Ser26) Antibody
Related articles to: ANXA2 (Phospho-Ser26) Antibody
- : Dietary cholesterol intake significantly influences liver health, yet the specific molecular mechanisms by which it accelerates fibrogenesis remain incompletely defined. This study aimed to characterize the dose-dependent effects of dietary cholesterol on hepatic injury and fibrogenesis, identify cholesterol-responsive gene networks through transcriptomic analysis, and investigate Annexin A2 (ANXA2) as a candidate molecular mediator linking dietary cholesterol to hepatic fibrosis progression. : A CCl-induced liver fibrosis mouse model was established and supplemented with dietary cholesterol (1-2%). Liver injury and fibrosis were assessed by liver-to-body weight ratios, serum biochemical markers, histological analysis, and fibrogenic gene expression. RNA sequencing combined with multiple hepatic fibrosis database analyses was performed to identify potential molecular mediators. : Dietary cholesterol supplementation aggravated CCl-induced hepatic fibrosis in mice, with dose-dependent increases in liver-to-body weight ratios and serum AST and ALT levels. Histological analysis showed enhanced collagen deposition and upregulation of fibrogenic genes. By integrating RNA-sequencing with multiple hepatic fibrosis database analysis and correlation analysis, we identified Annexin A2 (ANXA2) as a cholesterol-responsive gene associated with fibrosis. : Dietary cholesterol promotes liver fibrosis progression, and ANXA2 may act as a potential mediator linking cholesterol metabolism to hepatic fibrogenesis. - Source: PubMed
Publication date: 2026/05/15
Liu JiayangOu LingTai HaiyanChai YinghanTan LirongLin JieLi BingCao YingZhu Tingting - Cervical cancer is a gynecological malignancy closely associated with high-risk human papillomavirus infection. Trim45, a member of the E3 ubiquitin ligase family, is highly expressed in cervical cancer tissues; however, its specific mechanistic contribution to disease progression remains incompletely understood. By integrating single-cell sequencing, functional assays, and molecular profiling, we found that single-cell sequencing and IHC analyses revealed high Trim45 expression in cervical cancer tissues from patients with HPV-18 infection. Furthermore, we uncovered a novel mechanism by which Trim45 promotes cervical cancer progression: Trim45 suppresses the cGAS/STING signaling pathway activity by mediating ANXA2, which subsequently upregulates the expression of the key glycolytic enzymes HK2 and ENO2, enhances the aerobic glycolysis capacity of tumor cells, and ultimately promotes cervical cancer proliferation and metastasis. Collectively, these findings elucidate the molecular mechanism by which Trim45 drives the malignant progression of cervical cancer through the "ANXA2-cGAS/STING-glycolysis" axis. Statement of Integration, Innovation and Insight This study integrates single-cell sequencing and functional assays to reveal that Trim45, highly expressed in HPV-18 positive cervical cancer, suppresses the cGAS/STING innate immune signaling pathway by mediating ANXA2. This suppression subsequently upregulates the key glycolytic enzymes HK2 and ENO2, thereby enhancing aerobic glycolysis in tumor cells, and promotes proliferation and metastasis. These findings uncover a novel Trim45-ANXA2-cGAS/STING-glycolysis axis, offering potential therapeutic co-targets. - Source: PubMed
Zhang HuhuChen XiWang BanghuiLi LingxiDong XiaoleiZhang YimingLi Bing - Benign prostatic hyperplasia (BPH) is a prevalent age-related disorder characterized by chronic inflammation, metabolic dysregulation, and abnormal cellular proliferation. Protein lactylation, an emerging post-translational modification closely associated with cellular metabolism, has been implicated in the pathogenesis of various diseases. However, its role and associated molecular features in BPH remain uncharacterized. We integrated publicly available single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq datasets derived from BPH and normal prostate tissues. Utilizing machine learning algorithms (LASSO, Random Forest, and Boruta) strictly as feature selection tools, we identified key lactylation-related candidate genes. Subsequently, employing the BPH-1 cell line in vitro, we preliminarily investigated the potential biological functions of the prioritized epithelial target, ANXA2, through siRNA-mediated knockdown, Western blotting, ELISA, and cell proliferation assays. We computationally identified ANXA2 and IFI27 as key lactylation-related candidate genes, both of which were significantly downregulated in BPH tissues. scRNA-seq data revealed their cell-type specificity, demonstrating that ANXA2 is predominantly expressed in epithelial cells, whereas IFI27 is primarily expressed in endothelial cells. Furthermore, we uncovered a potential link between metabolism and inflammation involving ANXA2. Specifically, ANXA2 knockdown in BPH-1 cells was associated with alterations in glycolytic gene expression and a concomitant reduction in lactate production. Our data suggest that this decreased lactate level is associated with elevated secretion of the proinflammatory cytokine IL-6 and enhanced cellular proliferation. Additionally, cellular trajectory and communication analyses indicated that ANXA2⁺ epithelial cells and IFI27⁺ endothelial cells represent distinct subpopulations characterized by enhanced intercellular signaling capacities, suggesting their potential roles as critical molecular hubs within the BPH microenvironment. This study presents the first single-cell resolution landscape of lactylation-related gene activity in BPH. We computationally identified ANXA2 and IFI27 as key lactylation-related candidate genes. Importantly, our study suggests a potential link whereby ANXA2 deficiency is associated with BPH cell proliferation and potential metabolic and inflammatory alterations. These findings provide valuable new insights into the underlying pathophysiological mechanisms of BPH and lay the groundwork for the development of targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/05/25
Pang XiaotongZheng DeyongZhou RongbinDong KunWang Fubo - The limited understanding of keratinocyte-intrinsic pathways that drive and sustain inflammation in atopic dermatitis (AD) has hindered the development of targeted therapies. - Source: PubMed
Publication date: 2026/05/15
Zhang YuqiWang Ji-AnLi Long-FeiChen Xue-WenGui Qun-FengHe ChengZhu YuboTao YeMeng Jian-FengSong Meng-RuoSun RongWang JuanGuo Jian-ShuangLiu SuZhang Zhi-Jun - 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