Ask about this productRelated genes to: SNAG1 antibody
- Gene:
- SNX18 NIH gene
- Name:
- sorting nexin 18
- Previous symbol:
- SNAG1
- Synonyms:
- SH3PX2, SH3PXD3B
- Chromosome:
- 5q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-18
- Date modifiied:
- 2014-11-18
Related products to: SNAG1 antibody
Related articles to: SNAG1 antibody
- Extracellular vesicles (EVs) have emerged as key mediators of intercellular communication. However, the mechanisms governing their degradation remain poorly understood. In this study, we demonstrated that EVs are predominantly degraded via the lysosomal pathway. Mechanistically, MAP1LC3B recognizes SNX18 on the surface of endosome-escaped EVs to facilitate their sorting into the autolysosomal pathway for degradation. Leveraging this mechanism, we optimized the lysosomal sorting efficiency of EVs by surface display of LIR motifs and constructed an EV-based targeted protein degradation nanoplatform. The EV-based nanoplatform is highly modular and can be combined with monoclonal antibodies in a plug-and-play manner. It demonstrated remarkable efficiency and selectivity in degrading EGFR, PD-L1, and VEGF. Moreover, the nanoplatform demonstrated multi-targeting capability by simultaneously degrading EGFR and VEGF. Our findings uncover a previously unrecognized mechanism of EVs degradation and provide a novel strategy to harness the EVs degradation machinery as a nature-inspired nanoplatform for the degradation of multiple targeted proteins. - Source: PubMed
Publication date: 2026/04/02
Tong BideWang YuleiWei JunyuOu ZixuanLiang HuaizhenLei JieZhu DingchaoXu HanpengTan LeiLiao ZhiweiYang Cao - LPS-induced peritonitis is a prevalent clinical condition with incompletely understood underlying mechanisms. This study aimed to characterize the gene transcriptome and key proteins in the blood of mice with LPS-induced peritonitis. We established a mouse peritonitis model by administering LPS (10 mg/kg, i.p.) and collected blood samples (n = 6 per group) for bulk RNA sequencing. Through various bioinformatics approaches, we identified 290 differentially expressed genes (242 upregulated and 48 downregulated). Functional enrichment revealed the activation of inflammation-related pathways (e.g., NOD-like and Toll-like receptor signaling) and the suppression of adaptive immunity pathways (e.g., Th1/Th2 cell differentiation and T cell receptor signaling). From these, eight hub proteins (LDLR, FNBP1L, SNX18, FAM20C, INPP5F, PACSIN1, ZAP70, and SYNJ2) were identified, and their structural stability was confirmed via 300 ns molecular dynamics simulations. Critically, to validate our findings at the cellular level and in a clinical context, we further integrated four independent public single-cell RNA-sequencing datasets from human sepsis patients. This cross-platform analysis confirmed that the expression patterns of our hub genes are conserved in human patients with high cell-type specificity (e.g., ZAP70 downregulation in T cells and LDLR upregulation in monocytes). Moreover, a module score derived from these genes demonstrated strong clinical relevance, as it significantly distinguished sepsis patients from healthy controls and stratified clinical subtypes of sepsis. In conclusion, by integrating bulk transcriptomics, molecular dynamics, and cross-platform single-cell data, this research provides multi-scale insights into the systemic inflammatory mechanisms of peritonitis. It identifies therapeutic targets with clinical translational potential. - Source: PubMed
Publication date: 2025/10/30
Li HuijuanZhang JianfengSun Yulong - : Breast cancer (BC) is highly heterogeneous, with varying molecular characteristics, such as reliance on autophagy. Autophagy is a critical cellular degradation process that helps cells survive under stress, but its regulation can be influenced by altered microRNA (miRNA) expression. Studying miRNA changes during starvation-induced autophagy in both mammary epithelial cells and BC cells could reveal potential molecular therapy targets. : Rat mammary gland healthy epithelial and cancer cells were subjected to starvation, and differences in proliferation, migration, invasion, autophagy, and expression of autophagy-associated miRNAs were determined. Afterward, we assessed the effects of miR-218-5p modulation on the aforementioned processes. : Starvation-induced autophagy reduced the proliferation of all cells and increased the invasive and migratory capacity of cancer cells ( ≤ 0.05). We identified a miRNA signature related to starvation, comprising twenty-seven miRNAs. One miRNA had a significantly elevated baseline expression, while another six, including miR-218-5p, had a significantly lower basal expression in cancer cells compared to healthy cells ( ≤ 0.05). However, starvation caused significant miRNA expression changes, with miR-218-5p being upregulated specifically in cancer cells ( = 0.20-0.01). Functional studies on the role of miR-218-5p show that its inhibition decreases migration and leads to autophagosome accumulation. The study of miR-218-5p molecular targets has shown that its inhibition of sorting nexin 18 (SNX18) may act as an important regulator of the starvation-induced response in cancer cells. : The baseline expression of miRNA related to starvation and autophagy differs between rat mammary gland cancer and healthy cells. The response to starvation also varies between cancer cells and normal cells. Starvation induces BC-specific miRNA dysregulation, affecting particularly miR-218-5p, which acts via SNX18, promoting the cancer cells' survival. - Source: PubMed
Publication date: 2025/07/23
Gotowiec MateuszSmoliński AntoniMarcinkowska KatarzynaPascal WiktorWłodarski Paweł Krzysztof - Agonist-stimulated GPCR endocytosis typically occurs via the multi-faceted adaptor proteins known as βarrestins. However, endocytosis of several GPCRs occurs independently of β-arrestins, suggesting an additional mode of GPCR endocytosis, but the mechanisms remain unknown. Here we provide evidence that sorting nexin 9 (SNX9), a previously described endocytic remodeling protein, functions as a novel cargo adaptor that promotes agonist-stimulated GPCR endocytosis. We show that SNX9 and SNX18, but not β-arrestins, are necessary for endocytosis of the chemokine receptor CXCR4. SNX9 is recruited to CXCR4 at the plasma membrane and interacts directly with the carboxyl-terminal tail of the receptor in a phosphorylation-dependent manner. We also provide evidence that some receptors do not require SNX9 and SNX18 nor β-arrestins for endocytosis, suggesting additional modes for GPCR endocytosis. These results provide novel insights into the mechanisms regulating GPCR trafficking and broaden our overall understanding of GPCR regulation. - Source: PubMed
Publication date: 2024/11/07
Robleto Valeria LZhuo YaCrecelius Joseph MBenzow SaraMarchese Adriano - Di(2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause kidney damage. Green tea is among the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few studies have reported on GTP-relieving DEHP-induced kidney damage. - Source: PubMed
Publication date: 2023/09/21
Shi HengZhao XinhaiPeng QinZhou XianlingLiu SisiSun ChuanchuanCao QiuyuZhu ShipingSun Shengyun