Ask about this productRelated genes to: DCUN1D3 antibody
- Gene:
- DCUN1D3 NIH gene
- Name:
- defective in cullin neddylation 1 domain containing 3
- Previous symbol:
- -
- Synonyms:
- MGC48972, FLJ41725, DKFZp686O0290, SCCRO3
- Chromosome:
- 16p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-04
- Date modifiied:
- 2016-01-13
Related products to: DCUN1D3 antibody
Related articles to: DCUN1D3 antibody
- Pulmonary hypertension (PH) is a chronic and progressive disease that is characterized by increased pulmonary arterial blood pressure, causing heart strain and eventual heart failure. In the current study PH RNA sequencing (RNA-Seq) dataset involving 8 patients, consisting of 4 cases and 4 controls was selected for analysis. Pathway analysis revealed the involvement of the key genes in pathways crucial for PH. The protein-protein interaction (PPI) network analysis using the STRING database identified key hub genes that were significantly upregulated, including HAUS4, TUBB4A, TUBG1, NEED1, SASS6, NIN, DCUN1D3, CCDC22, ATP2B2 and LRRC37A. These hub gene-encoded proteins can be prominent drug targets for future interventions aimed at treating pulmonary hypertension. - Source: PubMed
Publication date: 2025/09/30
J Jino BlessyR JayasuryaMurugan ShanmugapriyaG Shirley Lois - Psoriasis is a chronic immune-mediated skin disease driven by the interleukin-23/interleukin-17 cytokine axis, yet its immunopathogenesis remains incompletely understood. Housekeeping genes, traditionally considered stably expressed across tissues and cell types, have not been systematically investigated for their role in psoriasis. Here, we aimed to identify psoriasis-associated housekeeping genes and explore their molecular mechanisms and clinical implications. - Source: PubMed
Publication date: 2025/09/01
Tang HaoWang JiachengZhang ShuhaoFeng GuanglongCheng XiangshuMeng XinChen RuiWang JiaqiJiang YongshuaiZhang RuijieLv Wenhua - DCUN1D3, a member of the DCNL (defective in cullin neddylation-like) protein family, has been implicated in ultraviolet (UV) radiation-induced cell cycle checkpoints, cell growth, survival, and neddylation. However, its specific function in male germ cells and potential involvement in spermatogenesis remain poorly understood. - Source: PubMed
Publication date: 2025/06/15
Liu MengGao WenxinSheng WenyiZhou NianchaoWu TiantianShen CongFeng GuannanXi Xiaoxue - Sleep restriction is associated with increased cardiovascular risk, which is more pronounced in female than male persons. We reported recently first causal evidence that mild, prolonged sleep restriction mimicking "real-life" conditions impairs endothelial function, a key step in the development and progression of cardiovascular disease, in healthy female persons. However, the underlying mechanisms are unclear. In model organisms, sleep restriction increases oxidative stress and upregulates antioxidant response via induction of the antioxidant regulator nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Here, we assessed directly endothelial cell oxidative stress and antioxidant responses in healthy female persons (n = 35) after 6 weeks of mild sleep restriction (1.5 h less than habitual sleep) using randomized crossover design. Sleep restriction markedly increased endothelial oxidative stress without upregulating antioxidant response. Using RNA-seq and a predicted protein-protein interaction database, we identified reduced expression of endothelial Defective in Cullin Neddylation-1 Domain Containing 3 (DCUN1D3), a protein that licenses Nrf2 antioxidant responses, as a mediator of impaired endothelial antioxidant response in sleep restriction. Thus, sleep restriction impairs clearance of endothelial oxidative stress that over time increases cardiovascular risk.Trial Registration: NCT02835261 . - Source: PubMed
Publication date: 2023/09/16
Shah RiddhiShah Vikash KumarEmin MemetGao SuSampogna Rosemary VAggarwal BrookeChang AudreySt-Onge Marie-PierreMalik VikasWang JianlongWei YingJelic Sanja - MicroRNAs (miRNAs) are critical in progression of bladder cancer (BCa). miRNA-93-5p is increased in cancers and is positively correlated with an unfavorable prognosis. But its effects on BCa remain rarely understood. This investigation aimed to dig out miRNA-93-5p affecting biological behaviors of BCa. In this research, mRNA and protein expression in cancer cells were assessed via quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell Counting Kit-8 (CCK-8), colony formation, scratch healing, and transwell assays were utilized to analyze cancer cell viability, colony-forming, migration, and invasion, respectively. Bioinformatics analysis predicted upstream regulatory genes and downstream target genes of miRNA-93-5p, with the targeting relationship being verified through a dual-luciferase assay. The BCa xenograft model in nude mice further investigated the effect of miRNA-93-5p and AND2-AS1 on tumor size and quality, and validated the relationship between HAND2-AS1/miRNA-93-5p/DCUN1D3. Our results displayed that miRNA-93-5p was increased in BCa cell lines. Knockdown miRNA-93-5p constrained BCa cell malignant phenotypes. HAND2-AS1 targeted miRNA-93-5p, thus restraining malignant progression of BCa cells. DCUN1D3 was found downstream of miRNA-93-5p. miRNA-93-5p modulated proliferation, migration, and invasion of BCa cells by targeting DCUN1D3. In vivo experiments disclosed that forced expression of lncRNA HAND2-AS1, and inhibited miRNA-93-5p regressed tumor growth. Meanwhile, the same as the results of cell experiments, the expression of miRNA-93-5p was downregulated, and DCUN1D3 expression was advanced in tumor tissues. To conclude, lncRNA HAND2-AS1 exerted anti-tumor effects and regulated BCa cell proliferation, invasion, and migration by targeting miRNA-93-5p/DCUN1D3. - Source: PubMed
Publication date: 2023/01/19
Wu XiangXu QingjiangLi TaoWei YongbaoZeng RongLin RongchengXu LinaYe LiefuLiu Zhihua