SNX9 ELISA kit
- Known as:
- SNX9 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-SNX9-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- SNX9 ELISA kit
Related genes to: SNX9 ELISA kit
- Gene:
- SNX9 NIH gene
- Name:
- sorting nexin 9
- Previous symbol:
- -
- Synonyms:
- SH3PX1, SDP1, SH3PXD3A
- Chromosome:
- 6q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2015-02-02
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- Mitochondrial-derived vesicles (MDVs) mediate selective trafficking of mitochondrial proteins and lipids to other organelles and contribute to organelle communication and mitochondrial quality control. While MDVs that deliver mitochondrial cargo to lysosomes have been extensively studied, the diversity of MDV pathways linking mitochondria to peroxisomes remains poorly understood. In particular, it is unclear how MDV pathways targeting peroxisomes relate to those delivering cargo to lysosomes, and whether cargos targeted to pre-existing peroxisomes utilize the same vesicular intermediates that participate in de novo peroxisome biogenesis. Here we examined MAPL trafficking using a peroxisome reconstitution system in PEX3-deficient fibroblasts. We found that MAPL is excluded from PEX3-positive pre-peroxisomal vesicles and instead is delivered to pre-existing peroxisomes, indicating that MAPL trafficking occurs through a pathway distinct from vesicles that initiate peroxisome formation. Structure-function analysis further revealed that a C-terminal amphipathic helix within MAPL is required for efficient targeting to peroxisomes. SNX9 depletion impaired both MAPL delivery to pre-existing peroxisomes and stress-induced lysosomal MDV pathways, whereas VPS35 depletion selectively reduced MAPL delivery without affecting lysosomal MDV pathways. In contrast, Parkin depletion impaired lysosomal MDV pathways but did not influence MAPL trafficking. Together, these findings demonstrate that mitochondria generate multiple classes of MDVs that are sorted into mechanistically distinct trafficking routes linking mitochondria with peroxisomes and lysosomes. - Source: PubMed
Publication date: 2026/05/12
Sugiura AyumuNakamura KohtaMcBride Heidi MOkazaki Yasushi - Hepatocellular carcinoma (HCC) is a highly aggressive primary liver malignancy characterized by limited therapeutic options and poor prognosis. Within the tumor microenvironment (TME), tumor-associated macrophages (TAMs) predominantly exhibit an M2-like phenotype, contributing to immune escape and tumor progression. Zymogen granule protein 16 (ZG16) has been reported to be downregulated in HCC, but its precise biological function and molecular mechanisms remain poorly understood. Therefore, we aimed to investigate the impact of ZG16 on HCC cell metastasis and TAM infiltration, as well as to elucidate its molecular mechanism. - Source: PubMed
Publication date: 2026/03/04
Meng HuiWang ZeyuanWang LiyeFang XiaokunLi HaonanMa WeiqianDing YiNan ManmanMeng YuLi LingLi YizhenChen KuishengZhang Mingzhi - NUMB is an endocytic protein with tumor suppressor activity, largely mediated by its ability to inhibit p53 degradation. This function depends on the inclusion of a short alternatively spliced exon (Ex3) in NUMB, although the mechanistic link between endocytosis and p53 regulation remains unclear. Here, we show that the Ex3-encoded sequence directs NUMB to the plasma membrane, where it forms a complex with the endocytic adaptor SNX9. This complex recruits p53 in an SNX9-dependent manner and is internalized and trafficked to multivesicular bodies, culminating in exosomal secretion, in a process requiring both SNX9 and NUMB. Exosomal p53 is taken up by recipient cells and translocated to the nucleus, where it activates p53-dependent transcriptional and phenotypic programs. These findings suggest that exosome-mediated p53 transfer may contribute to the establishment of a tumor-suppressive microenvironment. - Source: PubMed
Publication date: 2026/01/30
Cacciatore RobertaBasile AndreaFreddi StefanoSchiano Lomoriello IreneZucca Carlo RibelleCiossani GiuseppeScietti LuigiCuomo AlessandroRonzoni SimonaPelicci SimoneFaretta MarioZaccheroni ElenaPelicci GiulianaMatafora VittoriaBachi AngelaGunby Rosalind HelenPece SalvatoreSigismund SaraLanzetti LetiziaColaluca Ivan NicolaDi Fiore Pier Paolo - AIM2, an inflammasome sensor, has been extensively investigated for its ability to induce pyroptosis in macrophages. However, its role in the adaptive immune system remains poorly studied, particularly in B cells. AIM2 knockout mice had decreased follicular (FO) and marginal zone (MZ) B cell subsets and impaired IgG3 switching. The activation of B cells enhanced the co-localization of AIM2 and BCR. Interestingly, AIM2 exerts dual regulatory effects on BCR signaling transduction by positively regulating the PI3K-AKT signaling axis and negatively regulating the BTK-NFκB signaling axis. Through immunoprecipitation-mass spectrometry (IP-MS) analysis, SNX9 was identified as a critical molecule that promotes downstream signaling by facilitating the association of PI3K with CD19 in an AIM2-dependent manner. Furthermore, AIM2 is involved in the endocytosis of BCR and CD19 and the subsequent antigen uptake and presentation processes via SNX9-WASP interaction. In AIM2 knockout mice, this dual regulation leads to reduced overall BCR signaling characterized by decreased calcium signaling and reduced antibody production following RBD immunization. Conversely, AIM2 is overexpressed in B cells of Kawasaki disease patients, contributing to the development of this autoimmune disease. In summary, our study has unveiled a novel positive regulatory role of AIM2 in B cell receptor activation, endocytosis, and humoral response, focusing on AIM2-associated signaling pathways in B cells. - Source: PubMed
Publication date: 2025/12/23
Huang YanmeiGao PengyueLuo LiBai YuxinWang WeijiayiJiang PanpanZhang XinLai JuanLiu JuChang JiangDai XinLuo XiGuan FeiMiller HeatherDu XingrongLei JiahuiYang LuLiu Chaohong - Sorting nexin 9 () is involved in intracellular vesicle transport and signal transduction, and its abnormal expression is related to the occurrence and development of a variety of cancers. In lung adenocarcinoma (LUAD), the role and molecular mechanism of remain unclear. This study combined bioinformatics analysis and validation to explore its expression characteristics in LUAD, its specific effects on tumor development, and its potential molecular mechanism and prognostic value. - Source: PubMed
Publication date: 2025/11/26
Liu WeidiYin YichenWang BaozhenLi TaoChen Jing