Human DGCR8 cDNA Clone
- Known as:
- Human DGCR8 complementary Desoxyribonucleic acid Clone
- Catalog number:
- DC02831
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Human DGCR8 cDNA Clone
Related genes to: Human DGCR8 cDNA Clone
- Gene:
- DGCR8 NIH gene
- Name:
- DGCR8 microprocessor complex subunit
- Previous symbol:
- C22orf12
- Synonyms:
- DGCRK6, Gy1, pasha
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-29
- Date modifiied:
- 2019-01-25
Related products to: Human DGCR8 cDNA Clone
Related articles to: Human DGCR8 cDNA Clone
- ADAR1 is overexpressed in hepatocellular carcinoma (HCC) and has been linked to poor prognosis, metastasis, and recurrence; however, its precise functions and underlying mechanisms, particularly in the context of metastasis, remain inadequately elucidated. This study seeks to elucidate the functions and underlying mechanisms of the most abundantly expressed isoform of ADAR1, ADAR1p110, in the setting of HCC metastasis. In this study, hepatocyte-specific ADAR1p110 knock-in mice and engineered HCC cell lines were utilized to investigate the function of ADAR1p110 and . Genome sequencing, transcriptome sequencing, microRNA sequencing, RNA immunoprecipitation qPCR (RIP-qPCR), and RNA pull-down assays were performed to elucidate the mechanism of ADAR1p110 in HCC. We demonstrated that ADAR1p110 overexpression promotes HCC metastasis by improving the motility of HCC cells. Mechanistically, ADAR1p110 overexpression increases TUBA1A expression, which plays a crucial role in regulating HCC cell motility. At the molecular level, ADAR1p110 suppresses miR-451a biogenesis by competitively binding to pri-miR-451a, thereby preventing its cleavage by the Drosha/DGCR8 complex. Furthermore, we confirmed that TUBA1A is a direct downstream target of miR-451a. - Source: PubMed
Publication date: 2025/07/12
Sun LiangzhanYang HuiHu PengchaoZheng JingyiDu YuyangWu ShashaGao HanLuo HaoWang YanchenWang FenfenYan JingsongGuan Xin-YuanLi Yan - Silicosis, one of the most common and severe forms of pneumoconiosis, remains a major occupational health concern worldwide. Given the lack of effective therapies, understanding the underlying molecular mechanisms is urgently needed. Here, we report that ALKB homolog 1 (ALKBH1), an N6-methyladenosine (mA) demethylase, is upregulated in silica-induced pulmonary fibrosis and plays a pro-fibrotic role. The antifibrotic peptide Ac-SDKP inhibited Alkbh1 expression and alleviated pulmonary fibrosis. Mechanistically, ALKBH1 suppressed the biosynthesis of miR-129-5p by removing mA modification from pri-miR-129-5p, thereby reducing DGCR8-mediated processing and leading to decreased mature miR-129-5p levels. Ac-SDKP reversed this process, restoring miR-129-5p expression. Functionally, overexpression of miR-129-5p attenuated silica-induced pulmonary fibrosis by suppressing macrophage activation. Collectively, these findings identify the Ac-SDKP-ALKBH1-miR-129-5p axis as a critical regulatory mechanism, with ALKBH1-mediated mA demethylation of pri-miR-129-5p representing a key node and a promising therapeutic target for silicosis. - Source: PubMed
Li QianDu JiakunYi XueLi ShifengYang YiWang XinyuXu ZelinJin FuyuLi TianLi YaqianXu DingjieWei ZhongqiuCai WenchenMao NaZhang LijuanYu XiaoShi YiweiYang FangXu HongGao Xuemin - Overcoming chemoresistance is a major therapeutic challenge to improve patient's outcome, and lncRNAs are involved in the carcinogenesis and progression of NSCLC. Accordingly, this study was aimed to explore the roles and functions of lncRNA FENDRR in the progression and drug resistance of NSCLC. - Source: PubMed
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