AEBP1 antibody - N-terminal region (ARP31592_P050)
- Known as:
- AEBP1 (anti-) - N-terminal region (ARP31592_P050)
- Catalog number:
- arp31592_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- AEBP1 antibody - N-terminal region (ARP31592_P050)
Related genes to: AEBP1 antibody - N-terminal region (ARP31592_P050)
- Gene:
- AEBP1 NIH gene
- Name:
- AE binding protein 1
- Previous symbol:
- -
- Synonyms:
- ACLP
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-06
- Date modifiied:
- 2016-10-05
Related products to: AEBP1 antibody - N-terminal region (ARP31592_P050)
Related articles to: AEBP1 antibody - N-terminal region (ARP31592_P050)
- Osteoporosis (OP) and atherosclerosis (AS) are increasingly prevalent in aging populations and frequently coexist, sharing pathological features such as abnormal vascular calcification. However, the common marker genes underlying the crosstalk between OP and AS remain poorly understood. This study aimed to identify shared marker genes and cellular mechanisms contributing to the coexistence of OP and AS. Single-cell RNA sequencing (scRNA-seq) dataset and mRNA expression profiles related to OP and AS were obtained from the Gene Expression Omnibus (GEO) database. Bioinformatics analyses were performed using the R packages Seurat, AUCell, and hdWGCNA to identify circadian rhythm-related genes (CRGs) and associated cell populations. Naturally aged mice and a 0.25% adenine (AD)-induced mouse model were established. Micro-computed tomography (µCT), immunohistochemistry (IHC), immunofluorescence, Von Kossa staining, and RT-qPCR were conducted to experimentally validate the identified common genes. In human bone marrow samples, nine cell lineages comprising 17 subpopulations were identified, while six cell lineages comprising 18 subpopulations were identified in carotid artery samples. Circadian rhythm activity was significantly enriched in bone marrow stromal cells (BMSCs) in OP and vascular smooth muscle cells (VSMCs) in AS. By integrating scRNA-seq and bulk RNA-seq analyses, 69 common genes were identified, of which 15 hub genes were further selected through protein-protein interaction (PPI) network analysis. Experimental validation demonstrated that AEBP1 was markedly upregulated in both naturally aged and AD-induced mice, accompanied by increased PLIN1 expression, reduced osteocalcin (OCN) expression, and enhanced vascular calcification. This study reveals that circadian rhythm-related regulation of BMSCs in OP and VSMCs in AS plays a critical role in their coexistence. Furthermore, we identify shared marker genes, particularly AEBP1, which may serve as potential biomarkers and therapeutic targets for the concurrent development of OP and AS. - Source: PubMed
Publication date: 2026/03/27
Liu TengyanFan JiashuangFang JianyunQu ZhuanHe YaxinYang KaiYang JianlinZhang JuyeYang DanDai Lifen - Glioblastoma (GBM) is characterized by pronounced tumor heterogeneity and a complex immune microenvironment, contributing to poor patient survival outcomes. In this study, we comprehensively dissected the tumor microenvironment (TME) and uncovered potential molecular mechanisms by integrating single-cell, bulk, and spatial transcriptomic data. Hallmarks of malignancy and cell cycle regulatory pathways were consistently enriched across these modalities, promoting tumor cell proliferation and progression. Using machine learning algorithm, we identified seven hallmark-related prognostic signatures (HMsig), namely AEBP1, ASF1A, PRPS1, DCC, OPHN1, IL13RA2, and HDAC5-whose predictive importance was validated through SHAP analysis. Ligand-receptor (LR) interaction analysis further revealed that interactions involving OPHN1 were associated with poorer prognosis. Along the pseudotime trajectory of T-cell differentiation, immune checkpoint genes (ICGs) LAG3, PDCD1, and HAVCR2 were substantially upregulated. Notably, synergistic transcriptional regulation between tumor-related HMsig genes and ICGs in T cells was identified as a key factor influencing patient survival. Spatial transcriptomic analysis demonstrated the existence of synergistic gene interactions, deciphering the immunomodulatory functions of GBM biomarkers within the TME. - Source: PubMed
Publication date: 2026/03/25
Li TengyueMi WanqiYan HuaruiMa YiningJiang HanYang XiaoxuZhang YunpengHu Congxue - Astrocytes regulate brain cholesterol homeostasis, but the astrocyte-specific mechanisms disrupted in Alzheimer's disease (AD) are poorly understood. By integrating human bulk transcriptomes with single-nucleus RNA sequencing (RNA-seq), we identified adipocyte enhancer-binding protein 1 (AEBP1) as an astrocyte-enriched factor upregulated in AD. In postmortem human tissue and 5×FAD mice, astrocytic AEBP1 levels rise with age and disease progression. Astrocyte-specific AEBP1 knockdown ameliorates, while overexpression worsens, amyloid-β (Aβ) pathology in 5×FAD mice, confirming causality in vivo. In cultured astrocytes, AEBP1 overexpression represses lysosomal acid lipase (LIPA), leading to lipid droplet accumulation, excess cholesteryl ester storage, and lysosomal Aβ retention. LIPA restoration reverses these effects. Hippocampal transcriptomics and metabolomics from AEBP1-knockdown or LIPA-overexpressing 5×FAD mice show converged cholesterol/lipid pathway remodeling, reduced Aβ burden, and cognitive improvement. Mechanistically, AEBP1 sequesters NPAS3 in the cytoplasm, reducing its binding to the Lipa promoter. Thus, the astrocytic AEBP1-NPAS3-LIPA axis links lysosomal cholesterol catabolism to AD pathology. - Source: PubMed
Publication date: 2026/03/24
Wu JialinLu XiaonanZhang JienianWang ShuaihanLu ZeyuanHan YutongYang RuihanSu YiliangTan ChengHuo DianqiuLiu Yong USima Jian - Fatty acid metabolism (FAM) is essential for cancer cell proliferation and progression, contributing to membrane synthesis, energy storage, and signaling molecule production. However, effective therapeutic strategies targeting FAM are yet to be established in clinical practice. This study aimed to develop a novel FAM-related prognostic signature for bladder cancer (BLCA) and investigate its biological and clinical significance. - Source: PubMed
Publication date: 2026/02/27
Yu HuiLei QingqiangYang WenyongCao MinZhang MiaoyuWang TaisongDong JunhaoChen XueruiSu XuHuang YiXu HeZhuo HuiLin Liangbin - While the function of biglycan (BGN) is recognized in various cancers, its precise role and the mechanisms underlying cancer-associated fibroblasts (CAFs) formation within the melanoma tumor microenvironment (TME) remain poorly understood. Utilizing spatial transcriptomics, single-cell RNA sequencing (scRNA-seq), vitro/vivo assays, function analysis and molecular assays, this study comprehensively investigated the BGN regulatory network. We discovered that N6-methyladenosine (m6A) modulators-specifically YTHDF3, YTHDC1, and METTL14-cooperatively upregulate BGN expression in a parallel, non-hierarchical manner converging on functional m6A sites within melanoma cells. Consequently, BGN significantly promoted melanoma proliferation and metastasis. Within the TME, spatial transcriptomics and scRNA-seq revealed that CAFs, rather than tumor cells, exhibited the highest BGN expression. Cell trajectory analysis indicated that myCAFs may originate from iCAFs to interact with melanoma cells. Furthermore, midkine (MDK) signaling pathways was identified by cell chat analysis. Transcriptomic and spatial analysis revealed that BGN could regulate its expression at RNA and protein levels in CAFs through the regulator AE binding protein 1 (AEBP1). And the tumor promotion effect of CAFs may be executed by BGN/MDK axis, which also reduced CD8⁺ T cell infiltration in TME. Pharmacological inhibition of MDK also suppressed tumor growth with increased CD8⁺ T cell infiltration. Finally, this BGN/MDK axis could also drive the activation of normal fibroblasts into a CAF-like phenotype verified by vitro assays. In conclusion, the interplay between cancer cells and CAFs mediated by the BGN/MDK axis is a critical driver of malignancy in melanoma, highlighting it as a promising therapeutic target for intervention. - Source: PubMed
Publication date: 2026/03/15
Shi Hao-ZeWu Ming-YangLiu Jin-QuanTian CuicuiMa LiZhou Xue-MeiSun Ze-HaoXu Zhi-YongZhang Run-DongYe Shan-YuanHuang Li-MingWang YanXiong Jing-ShuBu Wen-BoCheng Xian-FengSun Jian-FangChen Hao