Ask about this productRelated genes to: AP2M1 antibody
- Gene:
- AP2M1 NIH gene
- Name:
- adaptor related protein complex 2 subunit mu 1
- Previous symbol:
- CLAPM1
- Synonyms:
- AP50, mu2
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-01
- Date modifiied:
- 2018-04-23
Related products to: AP2M1 antibody
Related articles to: AP2M1 antibody
- The absorption mechanism of cyclic peptides at the molecular level remains unclear. Previously, we found that flaxseed-derived cyclic peptide was absorbed into cells through endocytosis pathway dependent on clathrin. This study aimed to elucidate how CLQ triggers clathrin-mediated endocytosis. CLQ was labeled with FITC fluorescent probe, and results showed that CLQ was absorbed in a concentration- and time-dependent manner. Molecular docking, immunofluorescence colocalization and surface plasmon resonance showed that CLQ firmly binds to clathrin, even at the cellular level. The expression of key genes and proteins involved in clathrin-mediated endocytic vesicle formation was upregulated when cells absorbing CLQ, including CLTC, AP2M1, DNM2, and EPS15, whereas co-treatment with clathrin inhibitor (CPZ), this upregulation was suppressed. Above results suggested that CLQ binds with clathrin, then recruiting AP2M1, DNM2, and EPS15 to form endocytic vesicle, inducing the occurrence of clathrin-mediated endocytosis. These findings established a theoretical foundation for the development and utilization of dietary cyclic peptides. - Source: PubMed
Publication date: 2026/07/10
Nie YuwanZheng MiaoSun PeilongDeng ZeyuanYang KaiZou Xianguo - Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes severe encephalitis in humans and reproductive disorders in pigs. However, the host factors that regulate JEV infection and replication remain incompletely understood. - Source: PubMed
Publication date: 2026/08/07
Wei LongqinLi SaixiaoWang ChunyuZhao HongLuo WeiLi JinsongHuang LanzhenHuang XishiGu LantaoFang Qingli - Depression disproportionately affects women, yet the molecular adaptations underlying stress susceptibility in the female brain remain poorly understood. The nucleus accumbens (NAc) is a key brain region regulating reward, motivation and affective behavior and is strongly implicated in stress-related disorders. This study aimed to characterize proteome-wide molecular adaptations in the female NAc following chronic social stress. - Source: PubMed
Publication date: 2026/08/04
Patel ShashikantKushwaha RoliArvind AnushkaAnusha P VKumar ArvindIdris Mohammed MChakravarty Sumana - Defective intestinal epithelial tight junction (TJ) barrier function and endoplasmic reticulum (ER) stress are central pathological features of inflammatory bowel disease (IBD), yet the molecular mechanisms ER stress to TJ disruption remains poorly understood. Here, we investigated the role of autophagy in regulating intestinal TJ homeostasis during ER stress. ER stress was elevated in inflamed Crohn's disease tissue and chronic dextran sulfate sodium (DSS) colitis. In human intestinal epithelial Caco-2 monolayers, murine colon, and human colonic explants, induction of ER stress with tunicamycin, thapsigargin, or brefeldin A disrupted TJ barrier integrity, as demonstrated by reduced transepithelial electrical resistance and increased paracellular permeability. ER stress selectively increased the pore-forming TJ protein claudin-2 and altered occludin localization without significantly affecting other claudins. Pharmacologic activation of autophagy with rapamycin attenuated ER stress, restored TJ barrier function, reduced claudin-2 accumulation, and preserved occludin localization. Conversely, CRISPR-Cas9-mediated deletion of autophagy gene ATG7 exacerbated ER stress, apoptosis, and TJ barrier dysfunction in vitro, while intestinal epithelial-specific Atg7 knockout mice exhibited enhanced ER stress-induced intestinal permeability in-vivo. Mechanistically, prolonged ER stress impaired autophagic flux through IRE1α kinase signaling, resulting in accumulation of p62 and claudin-2. Inhibition of IRE1α kinase activity restored autophagy, reduced claudin-2 levels, and preserved TJ barrier function. We further identified adaptor-associated kinase 1 (AAK1) as a downstream mediator of IRE1α signaling during ER stress, with increased AP2M1 phosphorylation and altered claudin-2 trafficking. Claudin-2 overexpression alone induced ER stress and lysosomal damage, suggesting a feed-forward mechanism amplifying epithelial injury. Finally, enteric rapamycin administration reduced ER stress and restored autophagy in murine DSS colitis. Collectively, these findings identify an IRE1α-AAK1-autophagy axis as a critical regulator of intestinal TJ barrier integrity during ER stress. - Source: PubMed
Publication date: 2026/07/20
Arumugam PriyaSaha KushalGanapathy Ashwinkumar SubrameniumWang AlexandraHarris LeonardYochum GregoryNighot Prashant - Endocytosis regulates receptor trafficking and signaling, yet its role in colorectal cancer (CRC) remains unclear. We analyzed transcriptomic data from 15,025 CRC tumors to evaluate gene expression in clathrin-mediated endocytosis (CME) and the endosomal sorting complexes required for transport (ESCRT) pathway. Pathway-level signatures were compared across consensus molecular subtypes (CMS) and examined in relation to oncogenic signaling programs, while individual endocytosis-related genes were evaluated for associations with clinical outcomes in an independent randomized trial cohort. Expression of CME and ESCRT pathways varied by CMS, with the highest expression in CMS4 and the lowest in CMS3. Endocytosis signatures correlated with multiple oncogenic signaling pathways, including MAPK, TGF-β, WNT, PI3K, NOTCH, and angiogenesis, suggesting broad links between endocytic activity and tumor biology. In the randomized phase III CALGB/SWOG 80405 trial, low expression of -a core adaptor in the CME complex-was significantly associated with longer overall survival and progression-free survival in patients treated with anti-EGFR agents, but not in those receiving anti-VEGF agents. These findings suggest that endocytic trafficking may be associated with oncogenic signaling and differential therapeutic benefit in patients with metastatic CRC. The endocytosis pathway reflects biologically relevant heterogeneity in CRC and may help guide therapeutic stratification. - Source: PubMed
Publication date: 2026/07/05
Lenz HeinzArai HiroyukiElliott AndrewYang YanFarrell AlexMillstein JoshuaOu Fang-ShuInnocenti FedericoWang JingyuanBattaglin FrancescaJayachandran PriyaAlgaze SandraSoni ShivaniZhang WuGoldberg Richard MHall MichaelScott AaronHwang JimmyLou EmilWeinberg BenjaminMarshall John LGoel SanjayXiu JoanneKorn W MichaelVenook Alan