DGCR8
- Known as:
- DGCR8
- Catalog number:
- Y213628
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DGCR8
Related genes to: DGCR8
- 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: DGCR8
Related articles to: DGCR8
- Cardiac fibrosis is a pivotal pathological process driving adverse cardiac remodeling and a defining feature of end-stage heart disease. Nicotine, a principal constituent of tobacco products, is now recognized as an independent risk factor for cardiovascular disease. However, its direct effects on cardiac fibroblasts (CFs) biology and the molecular mechanisms underlying nicotine-induced cardiac fibrosis remain incompletely understood. - Source: PubMed
Publication date: 2026/04/27
Wu Hui-HuiLi Yue-YanMeng Fan-LiangDu Jia-MinZheng YanSong Chun-HongLi Li-MingLi YingSu Guo-Hai - Pluripotent stem cell (PSC) differentiation is orchestrated by intricate autocrine and paracrine signaling networks. Among these, exosomes, key components of the cellular secretome, are implicated as crucial mediators of intercellular communication via delivery of bioactive molecules, including microRNAs (miRNAs). This study investigated the role of exosomal miRNAs in stem cell differentiation using -deficient mouse embryonic stem cells (mESCs), which are incapable of producing mature miRNAs. Although the differentiation capacity was markedly impaired in these cells, partial restoration was observed following treatment with exosomes derived from differentiating wild-type mESCs. Exosomal miRNA uptake was confirmed, and gene ontology analysis revealed significant enrichment of pathways associated with cell fate determination, morphogenesis, and apoptosis regulation. Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that exosomal miRNAs modulated multiple osteoinductive signaling cascades, notably the MAPK and TGF-β pathways, in Dgcr8-deficient cells. Apoptotic markers were also downregulated, suggesting a protective effect conferred by the exosomal cargo. Collectively, our results suggest that exosome-mediated delivery of miRNAs may represent a fundamental mechanism by which pluripotent stem cells coordinate stress responses and differentiation trajectories, providing novel insights into the regulation of embryogenesis. - Source: PubMed
Publication date: 2026/03/25
Ha Tae-WonKim Hyun KyuNo DongyueLee Jeong BinKim AhyeonKim BomiSong YenaChoijamts MunkhzulChoi YoungsokLee MihyeLee Man Ryul - Legg-Calvé-Perthes disease (LCPD) remains a pediatric condition that causes hip joint deformities, with complicated pathogenesis. This study explored the influence of hypoxia-preconditioned human embryonic stem cells (hESCs)-derived exosomes on LCPD and its related mechanism. - Source: PubMed
Publication date: 2026/04/02
Luo TaoLiu QuanJiang XiaohuaZhou TonghuaJiang ShidingLiu GanganLan Xia - This study investigated associations between SNPs in miRNA-related genes (, , , ) and acute lymphoblastic leukemia (ALL) susceptibility in Chinese children and adolescents. - Source: PubMed
Publication date: 2026/04/02
Cao XiaoqingWang LingyunKang YurouTai PingChen NayunLiu YangYang YanliFang DaihuaHe Bangshun - N-methyladenosine (mA) RNA modification is a pivotal post-transcriptional regulator of RNA metabolism and cancer progression. Fat mass and obesity-associated protein (FTO), an mA demethylase, has emerged as a potent oncogenic driver across multiple malignancies. In this study, we demonstrate that FTO directly demethylates the primary transcripts of the miR-200b/a/429 cluster, thereby impeding DGCR8-mediated recognition and processing. The ensuing reduction in mature tumor-suppressive miR-200b/a/429 relieves repression of a suite of downstream targets intimately linked to metastasis and cell proliferation, ultimately accelerating tumor growth and lymph-node dissemination in esophageal squamous cell carcinoma (ESCC). Pharmacologic inhibition of FTO restores miR-200b/a/429 cluster expression and partially rescues the oncogenic phenotype elicited by FTO overexpression. Collectively, our findings uncover a previously unrecognized FTO-mA-miR-200b/a/429 axis that propels ESCC progression and highlight FTO as a promising therapeutic target for patients with ESCC. - Source: PubMed
Publication date: 2026/04/01
Zhou WeiWang ChunyanLi ChanghaoChen PengxiangLiu YuchenMao HongyuanZhu PengfeiGong YuxiaoCheng YufengZhang Lin