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)
- Tumor-associated macrophages (TAMs) play pivotal roles in shaping the tumor-microenvironment (TME) through functional plasticity, which is regulated by extrinsic and intrinsic signals. However, the role of vesicular trafficking in TAMs remains poorly understood. RAB31, a small GTPase enriched in myeloid cells, was proposed as a potential regulator of TAM polarization through clathrin-mediated endocytosis (CME). We hypothesized that RAB31 modulates TAM education by tumor-derived signals and thereby shapes antitumor immunity. - Source: PubMed
Publication date: 2026/09/02
Liu JingjingWang ShanshanBao DengyiDong GeMa YunxiZhang GuorongLiu XinZhang DongliWang LuluXu ShuqianCai Zhigang - Lung metastasis remains a determinant of poor prognosis and survival in breast cancer and is understood to depend on a permissive pulmonary immune niche rather than tumor cell traits alone. Here, we developed a host-directed RNA interference strategy to modulate this niche by reprogramming pulmonary B cells for breast cancer lung metastasis treatment. IF7C peptide-decorated cationic liposomes were constructed, which preferentially accumulated in the lung, and were internalized by pulmonary B cells, enabling selective silencing of annexin A1 (ANXA1). In tumor-conditioned primary B cells, ANXA1 knockdown reshaped the transcriptional landscape and shifted cytokine output away from an immunosuppressive profile characterized by IL-10, TGF-β, and IL-35. Functionally, ANXA1-silenced B cells lost their capacity to drive CD4⁺ T cells toward Foxp3⁺ regulatory differentiation and instead promoted Th1 features, while concurrently relieving suppression of CD8⁺ T-cell proliferation. In two postoperative syngeneic breast cancer models, perioperative administration achieved ANXA1 silencing in pulmonary B cells, reduced lung Treg accumulation, enhanced CD8⁺ T-cell infiltration and effector activity, and suppressed metastatic outgrowth with favorable systemic safety. These findings identify pulmonary B cells as an actionable regulator of the lung metastatic niche and establish perioperative, B-cell-focused ANXA1 silencing as a practical approach to prevent postoperative lung metastatic recurrence. - Source: PubMed
Publication date: 2026/08/29
Gao XiaokeZhang MengYao XiaohanWang JingWang XueyingLou XiaohanWan JiajiaDuan XixiZhang LijingLei NingjingHuang HefeiHuang SiyuanYan LinlinQin BoZhang JinkunQin ZhihaiWang Fazhan - Acute lung injury (ALI), a common respiratory disease with high morbidity and mortality, poses a serious public health threat. Apart from mechanical ventilation, limited safe and effective clinical therapies are available. Alisol B 23-acetate (AB23-a), one of the principal bioactive components of Rhizoma Alismatis, alleviates diverse inflammatory conditions, yet its role in LPS-induced ALI has not been reported. - Source: PubMed
Publication date: 2026/08/20
Liu SijinYang ChengfeiHuang ZiqiZhou MenglinZheng ZhiWang KaiLiao ShuangqingDai ZhuoxinXu Wen-WenLiu QuanxingDai Jigang - Although papillary thyroid carcinoma (PTC) is widely considered an immunologically cold tumor, detectable T-cell infiltration can influence disease progression in selected patients. Previous bulk analyses have linked cAMP-responsive element modulator (CREM) expression to a favorable progression-free interval and an inverse correlation with regulatory T-cell infiltration but have not resolved the cellular origin or functional state. In this study, we integrate single-cell RNA-sequencing data from a 23-sample PTC atlas with bulk Cancer Genome Atlas Thyroid Carcinoma (TCGA-THCA) validation. We show that CREM marks a T-cell receptor (TCR)-driven immediate early gene activation state in tumor-infiltrating T cells rather than a cAMP program; this state is consistently and modestly enriched within the FOXP3 regulatory T-cell compartment, challenging the interpretation that bulk inverse Treg-CREM correlations reflect Treg-intrinsic repression. CREM-high T cells upregulate ANXA1, and permutation-controlled analysis identifies a candidate paracrine axis from CD4/CD8 T cells to the epithelial epidermal growth factor receptor (EGFR). At the bulk level, CREM expression correlates with reduced proliferation programs and is associated with a prolonged progression-free interval (multivariate HR 0.56, 95% CI 0.31-1.00, = 0.050), with the effect direction preserved after immune and sex adjustment. Genome-wide differential expression and gene-set enrichment in an independent cohort (GSE193581) confirm that CREM-detected T cells are enriched for a TCR-driven immediate early transcriptional program, supporting the reinterpretation of CREM as a marker of TCR-driven IEG activation. - Source: PubMed
Publication date: 2026/08/18
Ling HaoQiu PeiyuHu YanzhuSun Yan - Head and neck cancer (HNC) is characterized by substantial immune heterogeneity and limited availability of clinically actionable molecular targets. Here, we developed an integrative single-cell eQTL-driven multi-omics framework to identify immune cell-specific causal genes and prioritize drug-repurposing candidates for HNC. - Source: PubMed
Publication date: 2026/08/06
Xue ZhangweiShen GuohangLin GongbiaoXue HanzhenWang RuoyanZhou YueChen YangWang KaiyongDai Yupei