Ask about this productRelated genes to: AP2A1 antibody
- Gene:
- AP2A1 NIH gene
- Name:
- adaptor related protein complex 2 subunit alpha 1
- Previous symbol:
- CLAPA1, ADTAA
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-01
- Date modifiied:
- 2018-04-23
Related products to: AP2A1 antibody
Related articles to: AP2A1 antibody
- Scale-drop disease virus (SDDV), a member of the genus Megalocytivirus, family Iridoviridae, causes severe disease outbreaks and significant economic losses in Asian seabass (Lates calcarifer) aquaculture. Despite its importance, the cellular mechanisms underlying SDDV entry into host cells remain poorly understood. In this study, we investigated the endocytic pathways involved in SDDV entry using a highly permissive Asian seabass kidney (ASBK) cell line. Pharmacological inhibition of clathrin-mediated endocytosis using chlorpromazine significantly reduced SDDV infection. In addition, inhibition of dynamin activity impaired viral entry, supporting a requirement for dynamin-dependent vesicle scission during internalization. Consistent with these findings, AP2A1, a core clathrin adaptor protein involved in clathrin-coated vesicle formation, was transiently upregulated during early infection. Cholesterol depletion by methyl-β-cyclodextrin (MβCD) markedly inhibited SDDV entry, whereas cholesterol replenishment restored viral infection, demonstrating a critical role for membrane cholesterol. In contrast, disruption of caveolae-mediated endocytosis or macropinocytosis had no significant effect on viral entry. Together, these results indicate that SDDV entry into ASBK cells occurs predominantly via a clathrin-mediated pathway that is dependent on membrane cholesterol and dynamin. This study provides new insight into the early host-virus interactions of SDDV and establishes a cellular platform for exploring host-directed intervention strategies against scale drop disease. - Source: PubMed
Publication date: 2026/05/21
Xin Ying LimChing Pei Carmen LeeXin Hong-YiPrabakaran Mookkan - Midkine (MDK), a secreted heparin-binding growth factor, is involved in tumor progression and metastasis. While serum MDK is widely recognized as a potential prognostic biomarker for colorectal cancer (CRC), its specific functional role and underlying mechanisms in CRC development are not fully understood. The four publicly available CRC microarray datasets-GSE41258, GSE44076, GSE81558, and GSE117606-along with TCGA-COAD and TCGA-READ datasets and their associated clinical data were obtained. MDK expression was measured at both the mRNA and protein levels using quantitative real-time PCR (qRT-PCR) and Western blotting. To investigate its oncogenic functions, a comprehensive set of assays was performed: transwell and wound healing assays for invasion and migration; CCK-8 and colony formation assays for proliferation; and tail vein/spleen injection models combined with xenograft models to study metastasis and tumor growth in vivo. To uncover underlying mechanisms, Western blotting was used to examine the involvement of epithelial-mesenchymal transition (EMT) and the PI3K/AKT signaling pathway. MDK is significantly overexpressed in CRC tissues and cells compared to normal tissues and cells. Notably, patients with high MDK levels show poorer overall survival (OS). Overexpression of MDK increases CRC invasion, migration, proliferation, and metastasis both in vivo and in vitro, while its knockdown reverses these effects. Mechanistically, MDK activates the PI3K/AKT pathway, leading to increased AP2A1 expression and promotion of EMT in CRC. MDK promotes invasion, migration, proliferation, metastasis, and EMT in CRC cells through the PI3K/AKT pathway by inducing AP2A1 expression, which could serve as a diagnostic marker. The PI3K inhibitor LY294002 significantly reduces AP2A1 levels and inhibits MDK-induced malignant behaviors. Targeting MDK-related signaling pathways may offer new strategies for CRC treatment. - Source: PubMed
Publication date: 2026/04/21
Li TengfeiXu ChengyuanGuo YangXu YanyanChen KaijiCheng YunshengGandhervin KesavamoorthyZhang JianmingLin Moubin - Fentanyl and its analogues are the most commonly used synthetic opioid analgesics in clinical practice, but their abuse is a significant concern. Drug-paired environmental cues often trigger memory retrieval, leading to relapse, complicating treatment and overdose prevention. In this study we investigated μ-opioid receptor-related molecular mechanisms underlying the retrieval of fentanyl contextual addiction memory in mice. A conditional place preference (CPP) model was established in mice by citrate injections of fentanyl (0.1 mg/kg) for 4 days. By performing whole-brain screening using c-Fos immunofluorescence staining, we found that the paraventricular thalamus (PVT) was dramatically activated. We conducted Western blotting, co-immunoprecipitation and proteomics to evaluate the proteins interacting with μ-opioid receptors on the membrane, and found marked externalization of μ-opioid receptors on the membrane in PVT neurons. We revealed that μ-opioid receptors trafficking in PVT was regulated by the extent of binding of Ap2a1 to the membrane μ-opioid receptors. By conditional knockdown and chemogenetic manipulation, we demonstrated the contribution of μ-opioid receptors to the retrieval of fentanyl contextual memory via modulating the neuronal activity in PVT. In conclusion, this study suggests that Ap2a1-mediated trafficking of μ-opioid receptors underlies the retrieval of fentanyl contextual addiction memory through regulating the neuronal activity in PVT. - Source: PubMed
Publication date: 2025/12/01
Li Yu-JieChen Ruo-SongZan Gui-YingSong Ying-CaiHuang Xue-YingZhang BingDu Wei-JiaYuan Ti-FeiLiu Zhi-Qiang - Fragile X syndrome (FXS), the most common inherited intellectual disability and monogenic cause of autism, results from loss of the protein fragile X messenger ribonucleoprotein (FMRP), which regulates mRNA translation essential for brain development and synaptic plasticity. FMRP has been implicated in the synaptic localization and surface expression of various membrane proteins, yet underlying mechanisms remain unclear. Here, we identified a broad dysregulation of membrane surface and associated proteins in FMRP-deficient neurons by quantitative mass spectrometry. Among them, we found increased steady-state levels of several subunits of the clathrin-adapter protein complex 2 (AP-2), including AP2A1 and AP2B1. We demonstrate that FMRP associates and represses translation of cognate mRNAs. Increased AP-2 in FXS models resulted in enhanced endocytosis of AP-2 cargoes, including dendritic AMPA receptors. These phenotypes were rescued by shRNA downregulation of AP2B1 to wild-type levels in FMRP-deficient neurons. These results reveal a novel translational mechanism controlling adapter dependent protein sorting in neuronal cells. - Source: PubMed
Publication date: 2025/07/05
Shi LiangKosti AdamRaj NishaSun JiarongGao YuhaoSimamora RoyValdez-Sinon Arielle NFaundez VictorBassell Gary J - Dysregulation retrograde axonal transport in neurons results in autophagosome accumulation, enhancing amyloid β (Aβ) production and accelerating Alzheimer’s disease (AD) progression. Ras-associated GTP-binding protein 7 (Rab7) is pivotal in autophagosome maturation and their fusion with lysosomes, as well as in bidirectional axonal transport through interactions with partner proteins. Recent studies suggest that adapter-associated protein complex 2 subunit α1 (AP2A1) modulates retrograde axonal autophagosomes transport, regulates autophagy, and influences AD progression. However, the interplay between AP2A1 and Rab7, along with the molecular mechanisms underlying their impact on neuronal autophagy in AD, remains poorly understood. - Source: PubMed
Publication date: 2025/06/09
Wang YangyangLi SiyuLiang XiaoFan JianingLi ShijieZhou FanlinLi XiaojuLai MengmengFeng DianmaoLi Yu