Ask about this productRelated genes to: NOSTRIN antibody
- Gene:
- NOSTRIN NIH gene
- Name:
- nitric oxide synthase trafficking
- Previous symbol:
- -
- Synonyms:
- MGC20702
- Chromosome:
- 2q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-06
- Date modifiied:
- 2016-10-05
Related products to: NOSTRIN antibody
Related articles to: NOSTRIN antibody
- Thoracic aortic aneurysm (TAA) is a potentially life-threatening degenerative disease whose principal danger arises from progressive aortic dilation with the attendant risk of rupture and dissection and which is characterized by extracellular matrix breakdown, smooth muscle loss, and endothelial dysfunction. Caveolae, plasma membrane microdomains built from caveolins (CAV1-3) and cavins (CAVIN1-4), govern nitric oxide (NO) signaling, endocytosis, and mechanotransduction. We hypothesized that downregulation of caveolae-associated genes, driven in part by microRNAs, contributes to endothelial failure and vascular remodeling in TAA. Normalized transcriptomic expression values for five caveolae-associated genes were retrieved from the GSE26155 dataset (43 TAA and 43 control aortas) using GEO2R. Differential expression was assessed for CAV1, CAV2, CAV3, CAVIN1, and CAVIN2, and Spearman correlation with Deming regression explored inter-gene relationships. Functional enrichment (Enrichr) and experimentally validated microRNA-target interactions (miRTarBase) were used to infer regulatory and mechanistic networks. CpG island mapping and gene-gene interactome construction (GeneMANIA) complemented the analyses. CAV1 and CAV2 were downregulated in TAA at nominal significance (CAV1, = 0.0225; CAV2, = 0.0361); after Benjamini-Hochberg correction across the five candidate genes both differences attenuated to a consistent trend ( approximately 0.09), while the two caveolins were strongly co-expressed (Spearman = 0.527, < 0.001; Deming CAV2 = 1.881 × CAV1-0.892), indicating coordinated transcriptional regulation. Network analysis linked both genes to NOS3, NOSTRIN, EGFR, HRAS, and RAC1, consistent with impaired endothelial nitric oxide and GTPase signaling. Gene Ontology enrichment highlighted endothelial proliferation, nitric oxide metabolism, calcium homeostasis, vesicle organization, and MAPK regulation. Database-supported analysis (miRTarBase) identified miR-93-5p, miR-199a-3p, miR-203a-3p, and the miR-29 family as experimentally validated candidate repressors of CAV1/CAV2. This integrative transcriptomic and microRNA analysis identifies coordinated CAV1 and CAV2 downregulation as a candidate molecular event in thoracic aortic aneurysm, associated with caveolar loss, endothelial dysfunction, and disrupted nitric oxide homeostasis. The CAV1/CAV2-microRNA axis represents a candidate mechanistic signature warranting further investigation as a potential therapeutic target in aortic disease. - Source: PubMed
Publication date: 2026/07/20
Magouliotis Dimitrios ESicouri SergeAndroutsopoulou VasilikiBaudo MassimoAthanasiou ThanosAvgerinos Dimitrios VSkoularigis JohnGiamouzis GrigoriosRamlawi BaselXanthopoulos Andrew - Hypoxia induces dynamic vascular adaptations that evolve over time and are further modified by reoxygenation. Although vascular responses are commonly described as either adaptive or maladaptive, the temporal progression of key endothelial signaling pathways remains incompletely integrated across the literature. This narrative review examines how vascular endothelial growth factor (VEGF-A), soluble fms-like tyrosine kinase-1 (sFlt-1), endothelial nitric oxide synthase (eNOS), nitric oxide (NO), nitric oxide synthase trafficking inducer (NOSTRIN), endothelin-1 (ET-1), and angiopoietin/Tie2 signaling contribute to vascular adaptation and dysfunction during acute, subacute, chronic hypoxia, and reoxygenation. - Source: PubMed
Publication date: 2026/07/11
Josef M S - Cervical squamous cell carcinoma (CESC) represents the second most commonly diagnosed malignancy among women worldwide, with substantial incidence and mortality rates, particularly in regions where breast cancer is not predominant. Recent advances in tumor-infiltrating lymphocyte (TIL) therapy have demonstrated promising clinical efficacy in CESC. This study elucidated the role of complement factor D (CFD) in CESC and evaluated its potential as a therapeutic target. Bioinformatic analysis of the GSE39001 dataset revealed significant downregulation of CFD in CESC tissues, a finding subsequently validated in 43 paired tumor and adjacent normal tissue samples. Functional assays demonstrated that CFD overexpression in CESC cell lines (SiHa and C33A) substantially suppressed cell proliferation, viability, and invasion, while concurrently attenuating CD8 + T cell exhaustion. Mechanistically, CFD overexpression upregulated nitric oxide synthase trafficking inducer (NOSTRIN) and suppressed the endothelial nitric oxide synthase (eNOS) signaling pathway, as confirmed through RNA sequencing and co-immunoprecipitation assays. Furthermore, the combination of TIL therapy with CFD overexpression significantly suppressed tumor growth in a PDX model. These findings identify CFD as a potential therapeutic target for CESC and suggest that CFD overexpression may enhance the efficacy of TIL therapy in this malignancy. - Source: PubMed
Publication date: 2026/06/02
Zhang WeiLi DongLiu ShanTang JiyingCai XiaojunZuo ZhigangLi ChaofuLiu YuhanZeng LanghongZhao Yi - Vasculogenic mimicry (VM) plays vital roles in tumor development that are closely relevant to patient adverse outcomes and chemoresistance. This study aimed to identify a novel VM-associated signature to forecast the prognosis and immunotherapy response of head and neck squamous cell carcinoma (HNSC) patients. - Source: PubMed
Publication date: 2026/04/30
Zhai YujiaGu XinyuHuang DiXue Miaomiao - Introduction Head and neck squamous cell carcinoma (HNSCC) is the most common cancer of the head and neck region, including the oral cavity, larynx, pharynx, nasal cavity, and paranasal sinuses. Cancer arises because of cumulative genetic and epigenetic alterations in cancer-associated genes. It is important to understand the genetic/epigenetic background of the tumors to establish molecular targeted therapies. So far, the knowledge of key genes or molecules, which are closely associated with the carcinogenesis and development of HNSCC, is insufficient for targeted therapies. On the other hand, recent advances in next-generation sequencing (NGS) have greatly contributed to cancer genome research. In this research, using RNA sequence data of HNSCC stored in The Cancer Genome Atlas (TCGA) database, we identified differentially expressed genes (DEGs), functionally enriched gene sets, and new prognostic markers or candidate therapeutic targets. This exploratory study investigated whether novel prognostic markers and candidate therapeutic targets for HNSCC could be identified from TCGA RNA-seq data. Methods The RNA sequence data were downloaded from TCGA, including 504 cases from cancer and 44 cases from corresponding normal tissue. The DEGs between cancer and normal samples were detected using the DESeq2 package in R software. Differences with | log2 fold change (FC) | > 1.0 and p-value <0.05 were considered as DEGs. Functional enrichment analyses were performed by ShinyGO 0.85 with Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. A gene set enrichment analysis (GSEA) was also performed using GSEA software. We also analyzed the top 10 up- and down-regulated genes, which were sorted by adjusted p-value, by using Kaplan-Meier analysis to assess their potential as prognostic markers. Results Using the DESeq2 package, 10,976 DEGs were detected, including 6,932 up-regulated genes and 4,044 down-regulated genes in cancer. As expected, functional enrichment analyses revealed enrichment of KEGG terms associated with cancers, including "Pathway in Cancer", "Human Papillomavirus infection", and "PI3K-Akt signaling pathway" in up-regulated genes, whereas KEGG terms enriched in down-regulated genes were mainly "Metabolic pathways". GO terms for "Cell differentiation (GOBP)" and "Extracellular region (GOCC)" were enriched both in up- and down-regulated genes, suggesting aberrant expression of genes associated with cell differentiation and remodeling of the extracellular matrix. GSEA data supported the enrichment analyses data. Kaplan-Meier analyses revealed that high expression of homeobox C6 () (p=0.048), nucleobindin 2 () (p=0.007), IL12A antisense RNA 1 () (p=0.001), calcium-binding protein 39-like ()(p=0.038) nitric oxide synthase traffickin () (p=0.024), SLC8A1 antisense RNA 1 () (p=0.016), were the significantly correlated with poorer prognosis. Conclusions Based on bioinformatical approaches, we identified significantly enriched gene sets and novel candidates for prognostic markers or therapeutic targets in HNSCC. Further investigation would aid in determining the anti-cancer effects of these candidates. - Source: PubMed
Publication date: 2025/10/14
Katase NaokiSakamoto YaeSuda HirokiMiyahara RinFujita Shuichi