AP1S1
- Known as:
- AP1S1
- Catalog number:
- 001718A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AP1S1
Related genes to: AP1S1
- Gene:
- AP1S1 NIH gene
- Name:
- adaptor related protein complex 1 subunit sigma 1
- Previous symbol:
- CLAPS1, EKV3
- Synonyms:
- AP19, SIGMA1A, WUGSC:H_DJ0747G18.2
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-01
- Date modifiied:
- 2019-04-23
Related products to: AP1S1
Related articles to: AP1S1
- Obesity is a major risk factor for metabolic syndrome, cancer, diabetes, and other diseases. The occurrence of comorbidities is associated with systemic and adipose tissue inflammation, which is marked by the presence of macrophages and neutrophils in adipose tissue. The role of neutrophils in driving adipose tissue inflammation and pathology is understudied and may hold therapeutic promise. MRP8 transgenic mice are frequently used to investigate neutrophil functions. A recent report demonstrates that the insertion of the MRP8 transgene resulted in whole-body deletion of Ap1s1 and Serpine1, the latter encoding the pro-obesogenic factor plasminogen activator inhibitor-1 (PAI-1). Here, we show that MRP8 transgenic mice have lower body weight than their littermate controls on a standard chow diet. Furthermore, they are resistant to weight gain, adipose tissue hypertrophy, systemic deregulation of glucose metabolism, infiltration of macrophages into AT, and liver steatosis upon feeding of obesogenic, high-fat diets (HFD). Mechanistically, this was independent of neutrophils or bone marrow-derived cells, sex, age of the mice, the duration of the HFD feeding, treatment start, housing facility, or the original source of the mice. The expression of Sepine1/PAI-1 and Ap1s1 is globally reduced across metabolic organs of MRP8 mice irrespective of diet, thus phenocopying previous reports of the obesity-protective effect of PAI-1 depletion in mice. Our findings demonstrate the limited applicability of MRP8 mice for obesity or metabolic studies due to the observed off-target effects and highlight the need for respective controls when using transgenic mice, such as Cre-only controls or use of independent Cre lines for studies involving the Cre/loxP system. - Source: PubMed
Forisch StephanSoltani FatemehSalvat Costa LaiaM Cardoso BeatrizMoreno Galiano YaizaDuval CedricAriëns Robert A SChandel Navdeep SKaartinen Mari TWculek Stefanie K - Breast cancer remains a leading cause of global cancer mortality, characterized by profound heterogeneity. While immune checkpoint blockade (ICB) has transformed oncology, its efficacy in breast cancer is often hindered by "immune-cold" microenvironments and immune exclusion. Programmed cell death (PCD) is a critical regulator of tumor immune microenvironment (TIME). However, its role in the breast cancer immune microenvironment remains poorly understood. - Source: PubMed
Wang GuixinCao JunmingKaysar ParhatLu ChengluChen ZiyiChen ZhaohuiZhang HanYu YueXie YongjieCheng ShanZhang PengpengWang Xin - Lung adenocarcinoma (LUAD), a leading type of non-small cell lung cancer, exhibits considerable molecular diversity due to genetic, epigenetic, and transcriptomic alterations, which affect tumour progression, treatment efficacy, and prognosis. This study systematically investigates non-synonymous single-nucleotide polymorphisms (nsSNPs) in potential biomarker genes AP1S1, CERCAM, and SLC34A2 using in silico approaches. Missense variants were obtained from Ensembl VEP (86 in AP1S1, 568 in CERCAM, 532 in SLC34A2) and assessed for their potential harm using SIFT, PolyPhen-2 (high damaging scores >0.85), and CADD (PHRED >30). FATHMM-CScape identified several high-confidence oncogenic mutations, while mCSM indicated stabilizing effects in most mutants (ΔΔG >0 kcal/mol), particularly in buried residues. AlphaFold structures were validated (Ramachandran favoured >92%), followed by homology modelling of mutants. Virtual screening of FDA-approved drugs identified Mitoxantrone (binding -10.4/-11.8 kcal/mol to AP1S1/CERCAM) and Rutin (-9.0 kcal/mol to SLC34A2), with significant hydrogen bonds (e.g., ASN135). MD simulations lasting 100 ns verified the stability of these complexes, indicating that AP1S1, CERCAM, and SLC34A2 could serve as potential biomarkers for LUAD. Additionally, Mitoxantrone and Rutin emerged as possible therapeutic candidates, necessitating further experimental validation. These findings elucidate the impact of mutations, contributing to precision oncology supporting these genes as potential LUAD biomarker candidates and suggesting Mitoxantrone and Rutin as promising compounds for further experimental evaluation. - Source: PubMed
Publication date: 2026/07/24
Robinson BinishaKushal AmishHanna Luke ElizabethPiramanayagam Shanmughavel - As a crucial type of post-translational modification, glycosylation plays a fundamental role in maintaining cellular homeostasis and is closely associated with the progression of Alzheimer's Disease (AD). Given the central involvement of the hippocampus in AD pathogenesis, elucidating the mechanisms of glycosylation in this brain region may provide critical insights and facilitate the development of precision medicine strategies for AD. We employed an integrated bioinformatics framework to identify glycosylation-related diagnostic biomarkers for AD. Limma and WGCNA were conducted on a hippocampal gene expression microarray dataset to detect glycosylation-associated DEGs, which were intersected with a glycosylation gene set obtained from GeneCards. Key diagnostic genes were selected using three machine learning algorithms in an independent cohort. The diagnostic model was subsequently validated in two additional independent microarrays datasets. Functional exploration and hippocampal heterogeneity were assessed at both bulk-tissue and single-cell levels. PPI analysis and NMF clustering further stratified AD patients into two subtypes. Finally, qRT-PCR validated the expression of biomarkers, and molecular docking based on the CTD suggested potential therapeutic candidates. Our analysis identified CKMT1B and AP1S1 as key downregulated glycosylation-related genes in AD. These genes were predominantly and highly enriched in hippocampal microglia at both bulk and single-cell levels and demonstrated strong diagnostic potential. PPI network analysis and NMF revealed that these hub genes could stratify AD patients into two distinct molecular subgroups. Furthermore, quercetin was identified as a potential multi-target therapeutic agent through database screening and CTD molecular docking studies. Collectively, this study bridges fundamental discovery with clinical translation by providing a diagnostic model, patient stratification subtypes, and a repositioned therapeutic candidate, outlining a promising path toward personalized AD management. - Source: PubMed
Publication date: 2026/05/24
Mu YunpingYu ShiqiYang ZhongruiChen ShenjieSun Jinlin - MiR-7847-3p is aberrantly expressed in multiple cancer types; however, its biological function and molecular mech anism in colorectal cancer (CRC) remain unclear. This investigation aims to explore the function of miR-7847-3p in CRC development and its potential regulatory mechanisms. - Source: PubMed
Publication date: 2026/01/05
Chen HaiqinWang YusenLu Ming