AP2m1 ELISA kit
- Known as:
- AP2m1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-AP2m1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- AP2m1 ELISA kit
Related genes to: AP2m1 ELISA kit
- 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
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- Enfortumab vedotin (NECTIN4-ADC), a NECTIN4-targeting antibody-drug conjugate, has shown substantial efficacy in urothelial carcinoma, yet primary and acquired resistance remain major barriers to durable benefit. By integrating paired spatial transcriptomic profiling of tumors collected before and after NECTIN4-ADC plus anti-PD1 therapy with humanized mouse models, single-cell RNA sequencing, and resistant cell systems, we mapped tumor-state remodeling during ADC resistance and identified a resistant tumor-cell population with increased NECTIN4 expression but defective ADC uptake. Mechanistically, AKR1C1 binds NECTIN4 and impairs the AP2M1-dependent clathrin-mediated internalization of NECTIN4-ADC, while the AKR1C1-WWP2 axis promotes extracellular vesicle-mediated ADC export and clearance, thereby reducing intracellular payload accumulation. Pharmacologic inhibition of AKR1C1 restores ADC uptake, increases payload delivery, and enhances therapeutic sensitivity in preclinical models. Together, these findings define a clinically relevant target-high but uptake-defective resistance state and establish altered membrane trafficking as a therapeutic target for overcoming ADC therapy failure in cancer. - Source: PubMed
Publication date: 2026/05/21
Wang YuzhaoChen ZibinWang WeikaiJiang LijuanLiang XiaoyuLiu ZhuoweiMa Zikun - Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen that poses a considerable threat to the global swine industry, particularly with emerging variants that complicate control efforts. However, the host factors involved in PRRSV entry are not well understood. In the present study, we identified members of the numb-associated kinase (NAK) family, specifically adaptor-associated kinase 1 (AAK1), G-associated kinase (GAK), and BMP-2-inducible kinase (BMP2K), as essential regulators of PRRSV entry utilizing both genetic and pharmacological approaches. Mechanistically, NAKs facilitate PRRSV entry by phosphorylating the adaptor protein complex 2 subunit mu-1 (AP2M1) at threonine 156, enhancing AP2M1 activation and thereby promoting its interaction with the YxxØ motif in PRRSV glycoprotein (GP) 5 and the receptor cluster of differentiation 163 (CD163). This interaction is critical for efficient trafficking of the virions to early endosomes (EEs). Disruption of AP2M1 phosphorylation or blockade of the AP2M1-YxxØ interaction significantly impaired PRRSV internalization, indicating the potential for targeting this pathway to inhibit infection. Notably, inhibition of the NAKs-AP2M1 axis effectively reduced infection across multiple PRRSV strains, highlighting its capacity as a broad-spectrum antiviral target. Collectively, our findings provide novel insights into PRRSV entry mechanisms and offer a promising therapeutic strategy to control emerging variants of this economically significant disease. - Source: PubMed
Publication date: 2026/04/13
Zhang LongxiangLi RuiYou LingqiaoJiang YanWang XinrongZhu JunhaiYan NanWang Yue - Alzheimer's Disease (AD) is among the most prevalent neurodegenerative disorders globally, yet effective early diagnostic strategies remain lacking. Advances in multi-omics technologies and the integration of artificial intelligence into medicine have created new opportunities for developing predictive models for AD. Biomarker-based models hold significant promise for enhancing early detection. In this study, we integrated multi-omics data to identify core risk genes with potential causal links to AD and developed an early diagnostic model, thereby providing a theoretical framework for precision intervention. - Source: PubMed
Publication date: 2026/03/24
Zhang YazhiLi ZiweiLi HanruiZhang Kuixing - Interstitial deletions involving 3q27.1 define a distinct microdeletion syndrome characterized by prenatal-onset growth restriction, postnatal microcephaly, hypotonia, intellectual disability, and distinctive craniofacial features. While AP2M1 haploinsufficiency has been proposed as the primary driver of this phenotype, the full spectrum of dosage-sensitive genes within the locus remains unclear. Here, we report a patient with a de novo heterozygous 3q27.1 microdeletion and delineate a refined minimal smallest region of overlap (SRO) of approximately 189 kb, representing the narrowest critical interval associated with the 3q27.1 microdeletion phenotype to date. Chromosomal microarray and exome-based CNV analysis confirmed the deletion, which encompasses PSMD2, EIF4G1, and POLR2H but excludes AP2M1 and DVL3. The patient exhibited severe intrauterine growth restriction, microcephaly, global developmental delay, and mild dysmorphism, consistent with the established 3q27.1 phenotype. PSMD2 encodes a non-ATPase regulatory subunit of the 26S proteasome, and its loss may disrupt proteasome-mediated protein turnover and neuronal homeostasis. Comparison with previously published cases and an overlapping ClinVar variant (ID: 60129) with similar features supports the pathogenicity of this minimal deletion. Our findings refine the 3q27.1 critical region, propose PSMD2 haploinsufficiency as a likely molecular mechanism underlying growth and neurodevelopmental defects. Further cases and functional studies are needed to confirm PSMD2 causality and clarify the proteasome-related mechanisms underlying 3q27.1 microdeletion syndrome. - Source: PubMed
Publication date: 2026/03/10
Uctepe EyyupEsen Fatma NisaMancilar HanifenurTümer SaitCelebi FahriYesilyurt Ahmet - Abnormal endocytosis of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) subunit GluA2 is implicated in early synaptic dysfunction in Alzheimer's disease (AD). In this study, we utilized human brain tissue samples from both male and female autopsy specimens (including 6 clinically diagnosed AD patients and 6 normal controls without central nervous system pathology), male and female 5 × FAD five-transgenic mice and their wild-type (WT) littermates (C57BL/6J genetic background), as well as mouse neuroblastoma Neuro-2a (N2A) cells, to demonstrate that GluA2 undergoes enhanced endocytosis in APP-overexpressing N2A cells. This enhanced endocytosis is driven by an increased interaction with the μ subunit of the adaptor protein complex 2 (AP2M1), without affecting total GluA2 protein levels. Targeting this interaction with the competitive peptide G2CT effectively restores GluA2 membrane expression and improves synaptic function in vivo. Furthermore, G2CT rescues cognitive deficits in male and female 5 × FAD AD mouse models, without detectable alterations in amyloid precursor protein processing or amyloid-beta (Aβ) production under the experimental conditions used. These findings identify the GluA2-AP2M1 interaction as a critical mechanism of early synaptic dysfunction and highlight a therapeutic strategy for AD that acts downstream of amyloid-β signaling and ameliorates synaptic and cognitive deficits without altering amyloid pathology. - Source: PubMed
Publication date: 2026/02/23
Xue MengtongPang YayanTian QiuyunDai ChunfangTian NaYuan HaoXu BoqingFan YepengPeng YiqingHao AiweiYan XiaoxinZhang QileiDong Zhifang