AP1M1
- Known as:
- AP1M1
- Catalog number:
- 001716A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AP1M1
Related genes to: AP1M1
- Gene:
- AP1M1 NIH gene
- Name:
- adaptor related protein complex 1 subunit mu 1
- Previous symbol:
- -
- Synonyms:
- AP47, CLAPM2
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-28
- Date modifiied:
- 2018-04-23
Related products to: AP1M1
Related articles to: AP1M1
- High‑risk (HR) human papillomaviruses (HPVs) rely on the continuous expression of the E6 and E7 oncoproteins to reshape epithelial biology, drive and sustain malignant transformation. The high‑risk E7 oncoprotein is multifunctional, and its phosphorylation by Casein Kinase II (CKII) is a key post translational modification that amplifies its oncogenic potential. Therefore, it is important to extensively delineate the consequences of E7 phosphorylation on HPV-driven transformation and malignant progression. Here, we identify Vangl1, a core planar cell polarity (PCP) scaffold protein, as a novel, phosphorylation‑dependent interactor of HPV‑16 E7. Through proteomics, biochemical and cell-based assays, this study established that CKII‑mediated phosphorylation is required for Vangl1 recruitment, and that this interaction is more pronounced with HPV‑16 E7, revealing a new mechanism by which HR HPVs might disrupt epithelial organization. In CaSki cells and ectopic expression models, E7 expression profoundly disrupts Vangl1 homeostasis, creating a biphasic proteostatic imbalance in which phosphorylated Vangl1 is aberrantly stabilised. This retention parallels E7 stability, revealing a reciprocal oncogenic stabilization. Furthermore, we found that Vangl1 is depleted in cytoskeletal cell fractions in the presence of E7, and that E7 translocates to membrane compartments where it colocalizes with Vangl1. In line with this, we identified that this abnormal Vangl1 stabilization occurs from its mislocalization and impaired trafficking arising from E7's interference with the Adaptor-Related Protein Complex 1 Subunit Mu 1 (AP1M1). Functionally, Vangl1 siRNA-mediated ablation in CaSki spheroids mirrors E6/E7 loss, leading to disrupted spheroidal architecture, reduced invasion, and increased sensitivity to chemotherapeutic stress. These phenotypes position Vangl1 as a key downstream effector through which E7 reshaped epithelial behaviour. Taken together, our findings reveal a CKII-dependent mechanism by which HPV-16 E7 hijacks a core planar polarity component to destabilize epithelial structure and promote malignant traits; thus, positioning Vangl1 as a potential druggable target in HPV-associated cervical cancer. - Source: PubMed
Publication date: 2026/09/21
Gbala Ifeoluwa DBasukala OmEl Abidine Amira ZineMyers Michael PBertolio RebeccaDel Sal GianninoBanks Lawrence - Lung cancer remains the leading cause of cancer mortality. The AP-1 adaptor complex, including AP1AR, AP1S1, AP1S2, AP1S3, AP1M1, AP1M2, AP1B1, and AP1G1, functions as a conserved hub of vesicular trafficking, selecting cargo and coordinating clathrin-mediated transport. By shaping receptor recycling, membrane composition, and signal duration, AP-1 influences core cancer phenotypes such as proliferation, migration, and therapy response. However, the family-level role of AP-1 adaptors in lung cancer is incompletely defined. We systematically profiled all eight AP-1 adaptor genes using multi-omics datasets, survival resources, pharmacogenomic panels, Human Protein Atlas data, pathway enrichment, and single-cell RNA sequencing with cell-cell communication modeling. was consistently upregulated in lung adenocarcinoma and independently associated with poorer overall survival. It was linked to cell-cycle progression, DNA replication checkpoints, hypoxia, and epithelial-to-mesenchymal transition (EMT). At single cell resolution, also regulate malignant epithelial and fibroblast cell types. Pseudotime analyses revealed progressive activation along proliferative and EMT axes, and CellChat modeling indicated enhanced stromal and epithelial signaling. and showed complementary roles, associated with oncogenic/inflammatory signaling and immune-metabolic programs, respectively. These findings identify as a clinically relevant biomarker and highlight AP-1 adaptor biology as an underexplored contributor to lung adenocarcinoma progression and therapeutic stratification. - Source: PubMed
Publication date: 2026/01/01
Solomon Dahlak DanielYeh I-JengLiu Hsin-LiangSu Che-YuLee Yung-KuoKo Ching-ChungLin Hui-RuKumar SachinXuan Do Thi MinhPalekkode NeethuFathima AymanLin Hung-YunWang Chih-YangYen Meng-Chi - This study employed a multi-omics approach to investigate the molecular and functional underpinnings of schizophrenia by integrating blood transcriptomic profiles, neuroimaging-derived brain phenotypes, and clinical symptomatology. RNA sequencing of blood samples from 43 patients with schizophrenia and 60 healthy controls identified 994 differentially expressed genes (DEGs), the vast majority of which were downregulated (n = 921, |FC| > 1.5, P < 0.05), with enrichment in pathways related to neuronal development and inflammation. Concurrent neuroimaging analyses revealed altered functional activation in key brain regions, including the prefrontal and anterior cingulate cortices. A Partial Least Squares correlation analysis demonstrated significant cross-modal relationships among gene expression, neuroimaging patterns, and clinical presentation. Furthermore, we identified six genes-GRK2, KLF3, TAOK2, ARFGAP45, AP1M1, and GPAT2-that were shared across gene sets associated with both brain function and clinical symptoms, suggesting a common transcriptional basis for these features of schizophrenia. Collectively, these findings provide novel insights into the integrated molecular and functional changes in schizophrenia, highlighting the value of a comprehensive multi-omics strategy to decipher its pathophysiology and potentially inform improved diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2025/11/21
Zhao Jia-NiWang Yun-QiLiu MinGuo Bao-BinWang You-RenGao BoLiu Miao-YanWu Wen-JunWu DiZhang Ya-HongYuan ZhenZhu LiMa Guo-LinCui Long-BiaoZhang Yue-Lang - Osteosarcoma, mainly arising from mesenchymal cells, is the most common bone tumor in children and adolescents, with high malignancy and a tendency for metastasis and recurrence. Epithelial cells undergoing epithelial-mesenchymal transition (EMT) often signal the start of tumor metastasis, as they gain mesenchymal characteristics that enhance their migration and invasion capabilities. - Source: PubMed
Publication date: 2025/09/04
Zhou FengXu XuezhengLuo YiLiu JianfanBu Jie - Anti-sense oligonucleotides (ASOs) are modified synthetic single-stranded molecules with enhanced stability, activity, and bioavailability. They associate with RNA through sequence complementarity and can reduce or alter mRNA expression upon binding of splice site positions. To target RNA in the nucleus or cytoplasm, ASOs must cross membranes, a poorly understood process. We performed an unbiased CRISPR/Cas9 knockout screen with a genetic splice reporter to identify genes that can increase or decrease ASO activity, resulting in the most comprehensive catalog of ASO-activity modifier genes. Here we reveal distinct targets, including AP1M1 and TBC1D23, linking ASO activity to transport of cargo between the Golgi and endosomes. AP1M1 absence strongly increases ASO activity by delaying endosome-to-lysosome transport in vitro and in vivo. Prolonged ASO residence time in the endosomal system may increase the likelihood of ASO escape. This insight into AP1M1 role in ASO trafficking suggests a way for enhancing the therapeutic efficacy of ASOs by manipulating the endolysosomal pathways. - Source: PubMed
Publication date: 2025/06/30
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