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)
- Annexin A1 (ANXA1) is a multifunctional regulatory protein involved in neuroinflammation and cellular homeostasis, but its role in amyotrophic lateral sclerosis (ALS) remains unclear. In this study, we investigated the relationship between ANXA1 and Hippo pathway signaling in ALS. Bioinformatic analysis of transcriptomic data from iPSC-derived motor neurons showed that ANXA1 expression was reduced in ALS and associated with apoptosis and Hippo pathway-related changes. Decreased ANXA1 expression was confirmed in hSOD1^G93A transgenic mice and NSC34 motor neuron-like cells. Phosphorylation levels of MST1/2, LATS1/2, and YAP1 were elevated, indicates activation of the Hippo pathway. Functional experiments showed that ANXA1 overexpression reduced Hippo pathway activation, enhanced cell viability, and decreased apoptosis, as increased Bcl-2 expression and reduced Bax and cleaved caspase-9 levels. In contrast, ANXA1 knockdown further activated Hippo pathway and aggravated apoptotic changes. These findings identify ANXA1 as an upstream regulator associated with Hippo pathway activation in ALS and suggest that the ANXA1/Hippo axis may represent a potential therapeutic target. - Source: PubMed
Publication date: 2026/08/17
Zhang YingDong XinyuShai YaoMasood AlamHan DidiHu YujingHe ZhonghuiZhou ZhenqiJiang Hongquan - Bovine leukemia virus (BLV) is an oncogenic retrovirus that naturally infects cattle. Once infected, the virus persists indefinitely throughout life at a transcriptionally silent stage. Soon after infection, humoral and cytotoxic activities efficiently abolish the viral replicative cycle, allowing only mitotic expansion of provirus-carrying cells. These anti-viral activities persist throughout the animal's life indicating that the immune system is permanently stimulated by BLV antigens. Although protein production is abolished during the chronic stage, viral transcription is not completely shut down. Extracellular vesicles (EVs) are nano-sized lipid bilayer vesicles released from most cells and play multiple roles in cell-to-cell communication, including immune modulation, angiogenesis, and transformation of cells by transferring genetic material and functional proteins. Colostrum is rich in EVs that carry bioactive proteins and RNAs reflecting maternal physiology and immune status. In this study, we aimed to characterize how BLV infection influences the protein cargo of colostrum-derived EVs. - Source: PubMed
Publication date: 2026/07/29
Pérez Cecilia ValeriaCarignano Hugo AdriánMarchetti Yamila CelesteGonzález Diego DanielRuiz VanesaTrono Karina GabrielaMongini Claudia - Calcification often occurs as a characteristic pathological manifestation in the progression of atherosclerosis (AS) plaques, but its mechanism is not fully understood yet. The purpose of this research was to supplement the exploration of key candidate genes and key cells involved in the calcification process of AS, building on existing insights into its underlying mechanisms. Through the examination of our internally generated single‑cell RNA sequencing (scRNA-seq) dataset derived from human carotid plaque samples, pivotal cellular populations associated with AS calcification were successfully identified. Following this identification, a comprehensive analytical approach was employed, incorporating differential gene expression profiling alongside the establishment of protein-protein interaction (PPI) networks, thereby enabling the extraction of critical genetic markers within these cellular subsets. Furthermore, a molecular regulatory framework was assembled, aiming to elucidate the mechanistic pathways through which these genetic determinants contribute to the calcification phenomena in AS pathology. Moreover, analysis of cell communication was applied to explore the interactions among cells. Pseudo-time analysis was employed to explore the expression of key candidate genes during the differentiation of key cells. Finally, monocytes were identified as key cells. WARS1, IFITM1, ANXA1, ADGRE2, and S100P were identified as key candidate genes. Moreover, 115 transcription factors such as THRB and 118 miRNAs such as hsa-miR-196a-5p were predicted to be associated with the key candidate genes. Across both calcified and non-calcified control specimens, the cellular communication between endothelial cells and natural killer (NK) T cell populations was consistently orchestrated via the PPBP-CXCR2 signaling axis. During monocytic differentiation trajectories, ADGRE2 expression exhibited a biphasic pattern characterized by initial gradual elevation followed by subsequent decline. Conversely, both ANXA1 and S100P demonstrated progressive upregulation throughout the differentiation process. The expression of IFITM1 and WARS1 first decreased, then increased, and finally decreased again. The present investigation successfully pinpointed five critical genes alongside one key cellular population, collectively providing potential molecular insights and candidate targets for further investigation into AS calcification. - Source: PubMed
Publication date: 2026/08/11
Yuan Huai WuWang WeiyeCheng WeiWang HongzheSong BoyanChen Tian XiangPeng Guo Ping - Relapsing polychondritis (RP) is a rare inflammatory disease characterized by recurrent cartilaginous inflammation with unclear pathogenesis. The precise alterations in the peripheral immune landscape driving RP pathogenesis remain incompletely defined. - Source: PubMed
Publication date: 2026/08/11
Lu ChenyangLiang YaoXu SiminXu WenyuJia XinleiZhu WeihangGu JieruoLiao ZetaoJiang Yutong - Differentiating Crohn's disease (CD) from ulcerative colitis (UC) is challenging, often resulting as Inflammatory bowel disease unclassified (IBDU). Based on targeted RNA sequencing, we recently reported a 3-gene signature algorithm that distinguished CD from UC. This study evaluated its ability to classify IBDU cases and explore disease biology. We analyzed 197 mucosal FFPE biopsies (inflamed and non-inflamed) from 113 individuals at diagnosis: CD (n = 42), UC (n = 41) and IBDU (n = 102; follow-up: 0-23 years (IQR)). Expression levels of ANXA1, PI3, and VDR mRNAs were measured by RT-qPCR, and assessed using logistic regression, and ROC curve analysis. The algorithm discriminated CD from UC with AUC values > 0.70 in 6 out of 8 patient subsets, peaking in inflamed adult biopsies (0.78, 95% CI: 0.64-0.92). At 80% sensitivity, specificity ranged from 46% to 58%, replicating previous cohort findings and confirming reproducibility. Application of the algorithm to the IBDU cases showed low classification accuracy, with frequent misclassification of cases that were later received definitive diagnoses. Incorporation of additional IBDU-specific features did not improve performance. While the 3-gene signature algorithm demonstrates moderate ability to distinguish CD from UC, its limited performance in IBDU cases highlights fundamental constraints of binary classification approaches in IBD. - Source: PubMed
James Jaslin PChristensen Ib JarleNielsen Boye SLangholz EbbeHøgdall EstridRiis Lene Buhl