DGCR6 Antibody
- Known as:
- DGCR6 Antibody
- Catalog number:
- XW-7945
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- DGCR6 Antibody
Related genes to: DGCR6 Antibody
- Gene:
- DGCR6 NIH gene
- Name:
- DiGeorge syndrome critical region gene 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-28
- Date modifiied:
- 2018-04-03
Related products to: DGCR6 Antibody
Related articles to: DGCR6 Antibody
- Glioma represents the most prevalent and aggressive primary brain tumor in humans. Tumor heterogeneity, the immunosuppressive tumor microenvironment, and therapeutic resistance contribute to the inevitable recurrence of gliomas, posing significant clinical challenges. Understanding the risk factors and molecular mechanisms underlying glioma recurrence and progression is critical for improving patient outcomes. In this study, we aimed to develop a recurrence-associated gene signature to predict clinical recurrence and survival outcomes while elucidating potential molecular mechanisms driving glioma recurrence. - Source: PubMed
Publication date: 2025/09/26
Li LanyingYang LeiZhang Yanfang - Imprinted genes are epigenetically regulated in normal tissues to follow monoallelic expression according to the parent of origin of each allele. Some of these patterns are dysregulated in cancer. - Source: PubMed
Publication date: 2025/05/25
Krushkal JuliaJensen Travis LWright GeorgeZhao Yingdong - Despite numerous studies demonstrate that genetics and epigenetics factors play important roles on smoking behavior, our understanding of their functional relevance and coordinated regulation remains largely unknown. Here we present a multiomics study on smoking behavior for Chinese smoker population with the goal of not only identifying smoking-associated functional variants but also deciphering the pathogenesis and mechanism underlying smoking behavior in this under-studied ethnic population. After whole-genome sequencing analysis of 1329 Chinese Han male samples in discovery phase and OpenArray analysis of 3744 samples in replication phase, we discovered that three novel variants located near FOXP1 (rs7635815), and between DGCR6 and PRODH (rs796774020), and in ARVCF (rs148582811) were significantly associated with smoking behavior. Subsequently cis-mQTL and cis-eQTL analysis indicated that these variants correlated significantly with the differential methylation regions (DMRs) or differential expressed genes (DEGs) located in the regions where these variants present. Finally, our in silico multiomics analysis revealed several hub genes, like DRD2, PTPRD, FOXP1, COMT, CTNNAP2, to be synergistic regulated each other in the etiology of smoking. - Source: PubMed
Publication date: 2024/05/24
Li Ming DLiu QiangShi XiaoqiangWang YanZhu ZhouhaiGuan YingHe JingminHan HaijunMao YingMa YunlongYuan WenjiYao JianhuaYang Zhongli - While extensively studied in clinical cohorts, the phenotypic consequences of 22q11.2 copy-number variants (CNVs) in the general population remain understudied. To address this gap, we performed a phenome-wide association scan in 405,324 unrelated UK Biobank (UKBB) participants by using CNV calls from genotyping array. We mapped 236 Human Phenotype Ontology terms linked to any of the 90 genes encompassed by the region to 170 UKBB traits and assessed the association between these traits and the copy-number state of 504 genotyping array probes in the region. We found significant associations for eight continuous and nine binary traits associated under different models (duplication-only, deletion-only, U-shape, and mirror models). The causal effect of the expression level of 22q11.2 genes on associated traits was assessed through transcriptome-wide Mendelian randomization (TWMR), revealing that increased expression of ARVCF increased BMI. Similarly, increased DGCR6 expression causally reduced mean platelet volume, in line with the corresponding CNV effect. Furthermore, cross-trait multivariable Mendelian randomization (MVMR) suggested a predominant role of genuine (horizontal) pleiotropy in the CNV region. Our findings show that within the general population, 22q11.2 CNVs are associated with traits previously linked to genes in the region, and duplications and deletions act upon traits in different fashions. We also showed that gain or loss of distinct segments within 22q11.2 may impact a trait under different association models. Our results have provided new insights to help further the understanding of the complex 22q11.2 region. - Source: PubMed
Publication date: 2023/01/26
Zamariolli MalúAuwerx ChiaraSadler Marie Cvan der Graaf AdriaanLepik KaidoSchoeler TabeaMoysés-Oliveira MarianaDantas Anelisa GMelaragno Maria IsabelKutalik Zoltán - Systemic autoimmune rheumatic diseases (SARDs) are a heterogeneous group of chronic multisystem inflammatory disorders that are thought to have a complex pathophysiology, which is not yet fully understood. Recently, the role of non-coding RNAs, including long non-coding RNA (lncRNA), has been of particular interest in the pathogenesis of SARDs. We aimed to summarize the potential roles of lncRNA in SARDs affecting the skin including, systemic sclerosis (SSc), dermatomyositis (DM) and cutaneous lupus erythematosus (CLE). We conducted a narrative review summarizing original articles published until July 19, 2021, regarding lncRNA associated with SSc, DM, and CLE. Several lncRNAs were hypothesized to play an important role in disease pathogenesis of SSc, DM and CLE. In SSc, Negative Regulator of IFN Response (NRIR) was thought to modulate Interferon (IFN) response in monocytes, anti-sense gene to X-inactivation specific transcript (TSIX) to regulate increased collagen stability, HOX transcript antisense RNA (HOTAIR) to increase numbers of myofibroblasts, OTUD6B-Anti-Sense RNA 1 to decrease fibroblast apoptosis, ncRNA00201 to regulate pathways in SSc pathogenesis and carcinogenesis, H19X potentiating TGF-β-driven extracellular matrix production, and finally PSMB8-AS1 potentiates IFN response. In DM, linc-DGCR6-1 expression was hypothesized to target the USP18 protein, a type 1 IFN-inducible protein that is considered a key regulator of IFN signaling. Additionally, AL136018.1 is suggested to regulate the expression Cathepsin G, which increases the permeability of vascular endothelial cells and the chemotaxis of inflammatory cells in peripheral blood and muscle tissue in DM. Lastly, lnc-MIPOL1-6 and lnc-DDX47-3 in discoid CLE were thought to be associated with the expression of chemokines, which are significant in Th1 mediated disease. In this review, we summarize the key lncRNAs that may drive pathogenesis of these connective tissue diseases and could potentially serve as therapeutic targets in the future. - Source: PubMed
Publication date: 2021/08/03
Muntyanu AnastasiyaLe MichelleRidha ZainabO'Brien ElizabethLitvinov Ivan VLefrançois PhilippeNetchiporouk Elena