ANPEP
- Known as:
- ANPEP
- Catalog number:
- 001683A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANPEP
Related genes to: ANPEP
- Gene:
- ANPEP NIH gene
- Name:
- alanyl aminopeptidase, membrane
- Previous symbol:
- CD13, PEPN
- Synonyms:
- LAP1, gp150, p150
- Chromosome:
- 15q26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-28
- Date modifiied:
- 2016-10-05
Related products to: ANPEP
Related articles to: ANPEP
- - Source: PubMed
Publication date: 2026/10/01
Wu YongkangZhang YankunShi XiaojiaWu MengtingSun MinFeng YingMa WenmengJiang XiuleFei DingqiZhao MingjianWu ZhuanchangLi ChunyangLiang XiaohongGao LifenMa ChunhongYue Xuetian - Esophageal adenocarcinoma (AC) incidence has increased markedly in the United States and other Western countries over recent decades. Gastro-esophageal reflux disease (GERD) can cause Barrett's esophagus, which is strongly associated with the development of AC. However, the mechanisms underlying the pathogenesis of AC remain poorly elucidated. In this exploratory pilot study, we performed transcriptomic profiling by RNA sequencing (RNA-seq) on six normal esophagus (WT), four Barrett's esophagus with low-grade dysplasia (BL), and six esophageal adenocarcinoma (AC) samples using RNA extracted via laser capture microdissection (LCM) of histologically confirmed formalin-fixed paraffin-embedded (FFPE) esophageal biopsies. Differential gene expression analysis demonstrated partial separation according to histological group, with overlap between BL and AC. BL and AC groups displayed a multitude of differentially expressed genes relative to WT samples; however, fewer differentially expressed genes were found when comparing BL and AC groups. We identified 3062 differentially expressed genes across comparisons (2289 WT vs. AC; 1854 WT vs. BL; 130 BL vs. AC). Using KEGG pathway analysis and functional annotation, candidate genes and pathways were identified. Genes related to the extracellular matrix, focal adhesion, and PI3K-AKT pathways were upregulated in BL and AC versus WT, while genes relating to keratinization, Ras/Rap1, and Hippo signaling were downregulated in BL and AC versus WT. A small set of genes (e.g., ANPEP, REG4, MEP1A) distinguished BL from AC and represent differentially expressed candidates for further investigation. This exploratory transcriptomic profiling provides insights into gene expression changes associated with AC pathogenesis and identifies candidate genes and pathways that warrant independent validation by qRT-PCR, immunohistochemistry, and functional studies. - Source: PubMed
Publication date: 2026/09/14
Hassan Md SazzadGuggenbiller MatthewRitter AnnieHeffernan ElizabethLi JunYan MinAwasthi Niranjanvon Holzen Urs - Avian infectious bronchitis virus (IBV) is endemic in poultry flocks worldwide, posing a significant threat to the global poultry industry. Frequent mixing of free-range local chickens with introduced chickens in Yunnan Province, China, facilitates the transmission, recombination, and mutation of avian IBV, thereby complicating disease prevention and control. In this study, we aimed to investigate the presence of IBV in poultry populations in Yunnan Province. Samples were collected from live poultry markets (LPMs) and breeding farms, comprising 725 randomly sampled cloacal/fecal swabs and 55 tissue samples. IBV-positive samples were confirmed via polymerase chain reaction (PCR), with an overall positivity rate of 0.89% (7/780) for all tested samples. The positivity rate was 0.35% (2/564) in Kunming, 3.7% (2/54) in Zhaotong, 20% (1/5) in Yuxi, and 12.5% (2/16) in Baoshan, while no IBV was detected in samples from Lanping, Xichou, or Ninglang. Six IBV strains, including five GI-19 strains and one GVI-1 strain, were successfully isolated. Phylogenetic analysis further showed that the Yunnan GI-19 strains predominantly clustered with strains originating from Sichuan Province. Sequencing of the S1 gene revealed several amino acids substitutions per isolate in hypervariable regions HVR1-HVR3. Notably, a valine (V) and glycine (G) insertion between amino acid positions 88 and 89 was identified exclusively in isolate F210, a feature rarely reported in IBV. Protein-protein docking analysis indicated that the unique 88-89 insertion in isolate F210 S1 may alter its binding interactions with the host receptor ANPEP. Whole-genome comparison revealed that isolate YX3 shared 97.05% nucleotide identity with strain CK/CH/GX/YL17/2017 from Guangxi, whereas isolates Q47, F13, and F210 shared 96.40%-97.27% identity with strain CK/Henan/H1036/2021 from Henan. Recombination analysis detected obvious recombination events in isolates F13, F210, Q47, and YX3, with GI-22 strains serving as the major parental donors. These genetic characteristics, recombination patterns, and structural insights demonstrate the complex evolutionary dynamics of circulating IBV strains in Yunnan. Continuous molecular epidemiological surveillance combined with functional protein analysis is essential to monitor emerging variants and formulating targeted, effective disease control strategies. - Source: PubMed
Publication date: 2026/09/03
Mu WeiwuLiu HuixinZou XuzhaoWang RonghaiWang JingxiaLi XianghuaHe FengpingAngkititrakul SunpethXiang BinYang Liangyu - The carcinogenic relevance of environmental contaminant bisphenol A (BPA) to colorectal cancer (CRC) has gained growing attention, yet the molecular networks potentially linking BPA exposure to CRC remain incompletely characterized. This study integrated network toxicology and machine learning to predict candidate molecular targets and putative signaling networks associated with BPA-correlated colorectal carcinogenesis. The study's methodology involved an initial differential expression screening across several CRC transcriptomic datasets to establish a disease-specific gene signature. Subsequently, a multi-tiered computational strategy was employed: network toxicology was used to map potential BPA-protein interactions, machine learning algorithms were applied to distill a minimal set of high-impact targets, and molecular docking simulations provided atomic-level validation of the proposed binding events. We identified 53 overlapping genes between predicted BPA-interacting proteins and CRC-related transcripts. Machine learning screening further filtered a 12-gene panel with favorable predictive performance for CRC status, including MET, SORD, DPEP1, KIT, RIPK2, SET, HSP90AB1, DBF4, MMP1, MMP12, ANPEP, and GLA. Molecular docking simulations predicted stable binding interactions between BPA and the protein products encoded by these 12 genes. This study delineates a specific gene network potentially targeted by BPA to promote CRC pathogenesis. The machine learning-derived 12-gene signature, interpreted as CRC-associated genes overlapping with predicted BPA targets and supported by in silico molecular docking, offers valuable insights into the molecular basis of BPA-associated colorectal carcinogenesis and presents candidate targets for subsequent experimental validation. - Source: PubMed
Publication date: 2026/08/16
Li XiaoxuanMai GenningXiao YuexiZhao RuijunHuang XiyueLi JunxiXiao YuchenDeng ZhujunLi MiaoXiong Wenjun - Liver metastasis is the leading cause of death in pancreatic ductal adenocarcinoma (PDAC), yet its molecular drivers remain poorly defined. Through integrated transcriptomic and proteomic screening of clinical specimens, we identify the membrane protein Cadherin-Related Family Member 2 (CDHR2) as a key orchestrator of hepatic colonization in PDAC. CDHR2 was upregulated in primary tumors versus adjacent tissues, further elevated in liver metastasis versus matched primary tumors, and markedly enriched in patient-derived plasma extracellular vesicles (EVs), peaking in patients with liver metastasis. Knockdown of CDHR2 in human PDAC cells suppressed proliferation, migration, and invasion, and in orthotopic models attenuated primary tumor growth, remodeled the tumor microenvironment, and reduced liver metastatic burden. Mechanistically, CDHR2 associated with PDK1 and promoted activation of the PDK1-AKT (Thr308) axis to drive proliferation. In turn, AKT activity correlated with the packaging of CDHR2 into EVs, coupling intrinsic signaling to EV cargo loading. Tumor-derived, CDHR2-enriched EVs formed a complex with Aminopeptidase N (ANPEP) on liver sinusoidal endothelial cells (LSECs), disrupting endothelial junctions and enhancing tumor-cell adhesion to enable transendothelial migration. Consistently, ANPEP inhibition or liver-specific knockdown curtailed hepatic colonization, whereas priming with CDHR2 EVs accelerated it. Finally, systemic delivery of EV-encapsulated siCDHR2 suppressed established primary tumors and markedly reduced liver metastasis. Collectively, our findings define a tumor-intrinsic CDHR2-PDK1-AKT (Thr308) axis coupled to an exosomal CDHR2-ANPEP endothelial-priming program and provide proof-of-concept for exosomal siCDHR2 as a candidate strategy against PDAC liver metastasis. - Source: PubMed
Publication date: 2026/08/04
Wang RuiWang YiXiao ShutingLiao ShuilinLiu SongsongChen XiZhou YinShan JingjingSong QibinWang HuaizhiChen QiangDong Ming