SNX17
- Known as:
- SNX17
- Catalog number:
- Y213609
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SNX17
Related genes to: SNX17
- Gene:
- SNX17 NIH gene
- Name:
- sorting nexin 17
- Previous symbol:
- -
- Synonyms:
- KIAA0064
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2015-02-16
Related products to: SNX17
Related articles to: SNX17
- While cisplatin is a widely used and effective chemotherapeutic agent in the treatment of head and neck squamous cell carcinoma (HNSCC), the molecular mechanisms underlying its resistance remain poorly understood. In this study, we identify OCIA domain containing 2 (OCIAD2) as a central mediator of chemoresistance and tumor progression in HNSCC. Through transcriptomic analysis and Co-immunoprecipitation coupled with mass spectrometry, we demonstrate that OCIAD2 modulates integrin signaling by directly interacting with integrin β1. Mechanistic investigations reveal that OCIAD2 does not regulate integrin β1 at the transcriptional level, but instead stabilizes its protein expression by preventing lysosomal degradation and enhancing its recycling. Importantly, OCIAD2 binds to SNX17 and enhances its association with integrin β1, promoting its recycling to lipid raft-enriched regions of the plasma membrane. By maintaining integrin β1 in these lipid raft compartments, OCIAD2 sustains the activation of the FAK-PI3K-AKT-mTOR signaling cascade, thereby fostering cellular resilience and resistance to cisplatin. Moreover, targeting OCIAD2, either through genetic silencing or RNA-based therapies, significantly sensitizes tumors to cisplatin treatment in preclinical models. This study uncovers a previously unrecognized trafficking-dependent mechanism of drug resistance, suggesting that OCIAD2 may serve as a novel therapeutic target to overcome chemoresistance in HNSCC. - Source: PubMed
Publication date: 2026/02/08
Cui LiSi ShanshanYe MinLin PeiZou MeiyanLin YunfanChen XuGuo BingSun WenjuanZhao Xinyuan - To investigate the genetic relationship between irritable bowel syndrome (IBS) and non-alcoholic fatty liver disease (NAFLD). - Source: PubMed
Publication date: 2025/12/15
Hong JundongJi RuiWang PeichengHuang FengmingZhang FanZhou YanlinLv Bin - Immune checkpoint blockade (ICB) faces limitations owing to high cost and restricted efficacy. This study identifies SNX17 as a key mediator of ICB resistance. Elevated SNX17 correlates with poor anti-PD-1 response in humans and mice. SNX17 deletion in tumor cells inhibits tumor growth via CD8 T cell-dependent mechanisms. SNX17 reduces uridine in the tumor microenvironment (TME), suppressing IFN-γ and upregulating PD1 in CD8 T cells. Exogenous uridine shows antitumor efficacy comparable to anti-PD-1/PD-L1 in low-SNX17 tumors and overcomes resistance in high-SNX17 models. Uridine enhances CD8 T cell function by promoting CD45 N-glycosylation and LCK phosphorylation. Mechanistically, SNX17 stabilizes RUNX2, promoting UPP1 transcription and uridine degradation in the TME. These findings position SNX17 as an ICB response biomarker and nominate uridine as a cost-effective immunotherapeutic strategy. - Source: PubMed
Publication date: 2025/12/29
Xiao JianbiaoLi ZhiyangDing YiZhu KejinZheng ZhihaoZhang YaoweiWeng JiawenWang FeifeiZhang YuqinZeng SisiQiu MinxingZhang ZhaowenWang ZhizhangLiang Li - Preeclampsia is a leading cause of maternal and perinatal morbidity associated with systemic lipid metabolism disturbances, yet the underlying molecular mechanisms remain incompletely understood. In this study, we integrated single-cell RNA-seq data from preeclamptic placentas with an in vitro hypoxia model to analyze gene expression changes across distinct trophoblast subpopulations. While all trophoblast lineages exhibited hypoxia-driven metabolic reprogramming, the response was highly cell-type specific. In the syncytiotrophoblast (SCT), the primary maternal-fetal barrier, preeclampsia was associated with a significant downregulation of LDLR and cholesterol biosynthesis genes (OR = 4.991, p = 6.30e-04). Concurrently, we observed increased expression of genes governing transcytosis (, ). In contrast, the extravillous trophoblast (EVT) displayed a divergent adaptive response, characterized by elevated LDLR expression and downregulated cholesterol biosynthesis. hypoxia modeling in BeWo b30 cells recapitulated the SCT-specific phenotype and identified a potential regulatory mechanism: a fivefold increase in expression (padj = 3.53e-10) and a 1.5-fold decrease in (padj = 1.76e-04)-key regulators that limit lipoprotein receptor recycling. This was accompanied by the suppression of lipid biosynthesis genes and the transcriptional activation of pathways associated with transcytosis and cholesterol efflux. Collectively, these results confirm the pivotal role of hypoxic stress in disrupting placental lipid metabolism and reveal a subpopulation-specific transcriptional program in preeclampsia-a shift from endocytosis to transcytosis-that likely serves as a compensatory mechanism to ensure fetal lipid supply under conditions of limited availability. - Source: PubMed
Publication date: 2025/12/09
Antipenko IvanKnyazev EvgenyKulagin TimurTonevitsky Alexander - Small GTP-binding proteins of the Rab, Arf, and Arf-like family mediate the recruitment of their effectors to subcellular membrane-bound compartments, which in turn mediate vesicle budding, motility, and tethering. Here, we report that Tectonin-β-propeller repeat containing protein 2 (TECPR2), a protein mutated in a form of hereditary sensory and autonomic neuropathy (HSAN), is an effector of early endosomal Rab protein, Rab5. We demonstrate that the HSAN-associated missense variants of TECPR2 are defective in Rab5 binding and, consequently, in membrane recruitment. Furthermore, our findings reveal that depletion of TECPR2 impairs recycling of a subset of cargo receptors, including α5β1 integrins, leading to their lysosomal degradation. TECPR2 interacts with SNX17 and subunits of the WASH complex, molecular players that regulate the formation of actin-dependent cargo retrieval subdomain on the early endosomes. Finally, we show that TECPR2 depletion in zebrafish embryos results in decreased survival, impaired movement and altered neuromuscular synaptic morphology. Our study suggests that TECPR2 functions as a linker between Rab5 and the actin-dependent cargo retrieval machinery, providing insights into how mutations in TECPR2 may result in a neurodegenerative disorder. - Source: PubMed
Publication date: 2025/11/26
Paul SankalitaPant RajatSharma PoonamWalia KshitizGupta SuhasiAseem AdhilBajwa Kamlesh KumariGeorge RubenVarma YudishBhatia TriptaRamachandran RajeshTuli AmitSharma Mahak