Ask about this productRelated genes to: SNX9 antibody
- 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 antibody
Related articles to: SNX9 antibody
- Sorting nexin 9 (SNX9) participates in endocytic trafficking and has been connected to several malignancies, but its involvement in breast cancer (BC) remains incompletely resolved. This work was designed to examine whether SNX9 supports BC progression and investigate signaling and cytoskeletal processes associated with its activity. The clinical relevance of SNX9 was assessed using bioinformatics analysis of publicly available cancer databases. Lentiviral vectors were used to establish BC cell models with stable SNX9 overexpression or knockdown. Both cellular (proliferation and motility) and murine (tumor growth and metastatic colonization) experiments were implemented to functionally characterize the SNX9-mediated phenotypes. The underlying mechanisms were investigated via western blotting, immunofluorescence, co-immunoprecipitation, and pathway-focused analyses. Across the analyzed datasets, greater SNX9 abundance was linked to worse overall survival outcomes in BC patients. Functionally, SNX9 upregulation conferred increased proliferative, migratory, and invasive capacities and contributed to both primary tumor enlargement and distant metastatic spread , whereas SNX9 depletion produced the reciprocal phenotypes. SNX9 silencing also increased the G2/M cell fraction and disrupted actin cytoskeletal organization mechanistically linked to reduced Ras-related C3 botulinum toxin substrate 1 (Rac1)/cell division cycle 42 homolog (Cdc42) activation and the subsequent impairment of lamellipodial and filopodial protrusion. Additionally, co-immunoprecipitation substantiated the physical coupling between SNX9 and the scaffold protein tyrosine kinase substrate with five SH3 domains (TKS5), which correlated with the invasive behavior of BC cells. Collectively, our findings establish SNX9 as a critical oncoprotein that drives BC progression by coordinating proliferative epidermal growth factor receptor (EGFR)/extracellular signal-regulated kinase 1/2 (ERK1/2) signaling and cytoskeletal dynamics through interactions with TKS5 and Rac1/Cdc42. Clinically, SNX9 qualifies as a promising prognostic classifier and a rational target for therapeutic intervention. - Source: PubMed
Publication date: 2026/09/14
Liu QingqingLi LeiGanesan KumarJiang YangZeng KewuSui YueGuan XinyuanHe RongfangChen Jianping - Late-onset Alzheimer's disease (LOAD) and major depressive disorder (MDD) share genetic etiologies. Here, we investigated brain transcriptomic landscapes to gain insights into shared and divergent molecular and biological etiologies across LOAD and MDD. - Source: PubMed
Lutz Michael WMan ZhaohuiChiba-Falek Ornit - Breast cancer is the most common cancer in women worldwide, and early detection remains a significant challenge. Recent studies have identified increased expression of Mammaglobin A (Q13296, Gene: ) mRNA in breast cancer, suggesting its potential as a disease marker, although its function is not fully understood. To elucidate Mammaglobin's role, this study sought to identify co-expressed miRNAs and analyze the biological pathways they regulate. - Source: PubMed
Publication date: 2026/09/01
Abella-Duque Juan FelipeLópez-Kleine LilianaParra-Medina RafaelRamírez-Clavijo SandraPayán-Gómez César - In brief: SNX9 is first shown to be essential for normal decidualization. Its downregulation in decidual tissue impairs trophoblast invasion and may underlie severe preeclampsia, revealing a new molecular pathway in this poorly understood dangerous pregnancy complication. Abstract: 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 that 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
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