Snx9 siRNA_Lentivectors
- Known as:
- Snx9 siRNA_Lentivectors
- Catalog number:
- i064350b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Snx9 siRNA_Lentivectors
Related genes to: Snx9 siRNA_Lentivectors
- 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
Related products to: Snx9 siRNA_Lentivectors
Related articles to: Snx9 siRNA_Lentivectors
- In acute pancreatitis (AP), the release of mitochondrial DNA (mtDNA) from pancreatic acinar cells (PACs) plays a pivotal role in triggering a lethal systemic inflammatory response. Despite the importance of mtDNA release, the regulatory mechanisms upstream of this event remain poorly understood, hindering the development of targeted therapeutic strategies. To address this, we utilized single-cell RNA sequencing, CUT&Tag, luciferase reporter assays, and experiments in a PAC-specific knockout mouse model to investigate the transcriptional program governing vesicle transport and mtDNA release in the context of AP. Our analysis revealed that vesicle transport pathways were activated in AP PACs and identified Runx1 as a core transcriptional regulator. We discovered that Runx1 directly binds and activates the Snx9 promoter. This interaction initiates a pathological cascade wherein Runx1-Snx9 signaling drives mitochondrial fragmentation and the biogenesis of intracellular mitochondrial-derived vesicles (MDVs). Under AP conditions, these MDVs are diverted from degradative pathways and routed to the secretory machinery to be released as pathogenic, extracellular mitochondrial-derived vesicles (Ex-MDVs). These Ex-MDVs were confirmed to be highly pathogenic, strongly activating the cGAS-STING pathway in macrophages. Notably, PAC-specific deletion of Runx1 in a mouse model significantly mitigated pancreatic injury and suppressed the systemic inflammatory storm associated with AP. This study is the first to elucidate the Runx1-Snx9 transcriptional axis as the core upstream mechanism responsible for the anomalous generation and secretion of Ex-MDVs from PACs during AP, providing novel insights into AP pathogenesis and identifying this axis as a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/16
Gao MengqiXiao GuohuiChen KunhaoLi ShiyuChen CongYu SifeiWu YahuiYang KaigeXie RongliChen ErzhenJiang JianChen YingFei JianMao EnqiangXu Dan - Aim of the study was to investigate the roles and interaction mechanisms of RAB40C and SNX9 in prostate adenocarcinoma (PRAD) progression and their impact on the Hippo signaling pathway. PRAD is a significant health concern, and understanding the molecular underpinnings is essential for its effective management. Objective of this study was to identify key genes and pathways involved in PRAD using weighted gene co-expression network analysis (WGCNA) and determine the functional implications of RAB40C and its relationship with SNX9. - Source: PubMed
Publication date: 2026/01/23
Qin LiangYang NingYang FanLu XuweiWu JiawenGuo Zhuifeng - T cell exhaustion (Tex) severely limits the efficacy of tumor immunotherapy, yet strategies targeting its upstream regulatory mechanisms remain underexplored. In this study, a targeted nanodelivery system, CD8a-RM-MOF@siSNX9, was developed to preferentially enrich siRNA delivery in CD8 T cells and evaluate its potential to reverse Tex in triple-negative breast cancer (TNBC). Using a 4T1-induced TNBC mouse model combined with RNA sequencing analysis, SNX9 was identified as a key regulator associated with Tex. Silencing SNX9 was accompanied by reduced NFATc2-NR4A1-TOX signaling, decreased exhaustion phenotypes, and enhanced cytokine secretion and cytotoxic activity of CD8 T cells. The nanoplatform exhibited prolonged circulation in vivo (t₁/₂ ≈ 12.4 h) and efficient tumor-targeted accumulation (~ 8.5%ID/g). Importantly, the nanoparticles preferentially accumulated in CD8 T cells within the tumor microenvironment, leading to SNX9 knockdown, attenuation of the NFATc2-NR4A1-TOX regulatory program, reversal of Tex, and significant suppression of TNBC tumor growth while maintaining favorable biosafety. Collectively, these findings demonstrate that CD8a-RM-MOF@siSNX9 represents a promising targeted siRNA delivery platform with preferential CD8 T-cell enrichment for targeting Tex and enhancing antitumor immunity in TNBC. - Source: PubMed
Publication date: 2026/06/04
Hu WeiChen QishuaiMa YanLiu YangQiu ShushengDong XianingZhu ZengjunWu XuanxuanDu JianxinXu YanbinTian MaojinZhao Peiqing - 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