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 co-occurrence of nanoplastics and heavy metals like lead (Pb) in the environment presents a significant neurotoxic risk, yet the mechanistic basis for their combined effects remains poorly defined. In this study, we investigated the combined neurotoxic effects of 50 nm polystyrene nanoplastics (PS-NPs) and Pb in mouse hippocampal HT22 cells. Co-exposure to PS-NPs (50 μg/mL) and Pb (10 μg/mL)-concentrations commonly used in in vitro mechanistic studies-for 24 h, but not individual treatments, enhanced cytotoxicity and induced ferroptosis-related features, including iron metabolism dysregulation, lipid peroxidation, antioxidant defense impairment, and mitochondrial damage. Furthermore, the ferroptosis inhibitor Ferrostatin-1 (Fer-1) attenuated cell death, supporting ferroptosis as an important contributor to the observed cytotoxicity. Transcriptomic analysis revealed significant alterations in ferroptosis-related pathways, with selected differentially expressed genes validated by qRT-PCR. Physicochemical characterization (DLS/zeta potential) revealed changes in the hydrodynamic size and zeta potential of PS-NPs following incubation with Pb, while ICP-OES analysis of the supernatant provided evidence for the association of Pb with PS-NPs. This enhanced toxicity was associated with increased intracellular Pb accumulation facilitated by PS-NPs, involving the clathrin-mediated endocytosis (CME) pathway, as indicated by upregulation of key CME-related proteins (CHC, AP2M1, and Dynamin 2) and enhanced CHC-AP2M1 co-localization. Pharmacological inhibition of CME using chlorpromazine (CPZ) effectively reduced Pb uptake and attenuated ferroptosis-related cellular damage. Our findings provide insights into a proposed CME-associated Trojan horse-like mechanism whereby PS-NPs enhance ferroptosis-related neuronal responses to Pb exposure, highlighting the potential implications of nanoplastic-heavy metal co-exposure for environmental health. - Source: PubMed
Publication date: 2026/09/22
Yue LuLi QianLiu TaoDu QianHu YanjingWei DongqiongHuang DejunQi Yongmei - 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