Antibodies: SNX9 HOST: Goat Clonality: pAb
- Known as:
- Antibodies: SNX9 HOST: Goat Clonality: pAb
- Catalog number:
- CA18268-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biomatic
- Gene target:
- Antibodies: SNX9 HOST: Goat Clonality: pAb
Related genes to: Antibodies: SNX9 HOST: Goat Clonality: pAb
- Gene:
- CERNA2 NIH gene
- Name:
- competing endogenous lncRNA 2 for microRNA let-7b
- Previous symbol:
- -
- Synonyms:
- HOST2
- Chromosome:
- 10q23.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2017-04-27
- Date modifiied:
- 2017-07-14
- 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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- Preeclampsia (PE) is a gestational hypertension disorder emerging after 20 weeks of pregnancy, complicating 5-8% of pregnancies and representing a leading cause of maternal-fetal morbidity and mortality. Despite its clinical significance, the etiology and pathogenesis of PE remain obscure. Sorting nexin 9 (SNX9), a key regulator of intracellular trafficking and endomembrane dynamics, has been poorly explored in reproductive physiology. This study investigates the role of SNX9 in PE, demonstrating significant downregulation of SNX9 in decidual tissues from preeclamptic patients. In vitro decidualization models showed SNX9 expression correlated with decidualization progression, as evidenced by upregulation of decidual markers (IGFBP1, PRL), while SNX9 knockdown impaired decidualization. Transwell assays revealed that aberrant SNX9 expression restricted trophoblast invasion into endometrial stromal cells. In pregnant mice, SNX9 expression in decidual tissues positively correlated with decidualization regulators (Wnt4, Bmp2) and markers (Prl8a2, Dtprp). Consistent expression patterns were observed in pseudopregnant mice after artificial decidualization induction, excluding embryonic influences. Collectively, these findings establish SNX9 as essential for normal decidualization, with dysregulated SNX9 potentially contributing to PE pathogenesis. This study uncovers a novel link between endomembrane dynamics and PE, providing insights into its molecular mechanisms. - Source: PubMed
Publication date: 2026/08/06
Wang KaixuanFu RuiXu YanxinZhang Cong - Urinary proteomic profiling (UPP) provides insights in disease mechanisms and origin of symptoms. Using UPP, this study aimed at deepening insight in the biology of exercise tolerance. - Source: PubMed
Publication date: 2026/07/30
Liu Chu-HaoMartens Dries SAn De-WeiSiwy JustynaLatosinska AgnieszkaPellicori PierpaoloVerdonschot Job A JAhmed Fozia ZWei Fang-FeiRossignol PatrickPetutschnigg JohannesHeymans StephaneCuthbert Joe JYu Yu-LingGirerd NicolasClark Andrew LVerhamme PeterZhang Dong-YanLi YanNawrot Tim SCleland John GZannad FaiezMischak HaraldStaessen Jan A - Collective endothelial migration during vascular development relies on dynamic cell-cell contacts, yet how the junctions between leader and follower cells are organized remains poorly understood. Using Cryo-SIM followed by FIB-SEM, we investigated the nanoscale 3D ultrastructure of asymmetric adherens junctions (AAJs), revealing a wide spectrum of membrane folds at the contact interface between migrating endothelial cells. By performing a junction localization screen, we identified a variety of membrane curvature-sensing BAR domain proteins selectively enriched at AAJs. Among these, BIN1 and SNX9 emerged as novel regulators of front-to-rear polarity in follower cells during endothelial collective migration. The spatiotemporal recruitment of these individual BAR proteins associated with distinct phases of AAJ remodeling. Furthermore, depletion of SNX9 disturbed VE-cadherin dynamics, endothelial cell directionality, and sheet migration in the common cardinal vein of zebrafish. These findings highlight junctional nanoscale membrane curvatures as hubs for the spatiotemporal recruitment of a repertoire of BAR proteins to remodel AAJs and guide collective endothelial migration during vascular development. - Source: PubMed
Publication date: 2026/07/27
Janssen Verade Kraker HannahAaron Jesse Sde Haan Annettde Heer IrisKhuon SatyaDa Silva JasonDriessen Amber J MChew Teng-LeongTan Josephine M ELagendijk Anne KAngulo-Urarte AnaHuveneers Stephan - 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