DGCR8 _ Pasha
- Known as:
- DGCR8 _ Pasha
- Catalog number:
- Y214214
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DGCR8 _ Pasha
Related genes to: DGCR8 _ Pasha
- 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 _ Pasha
Related articles to: DGCR8 _ Pasha
- 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 - In 85% of cases, kidney tumours in children are represented by nephroblastoma or Wilms' tumour. Children are treated according to protocols developed by SIOP-RTSG in Europe and several other continents and by NWTSG-COG in North America. The SIOP-RTSG protocol includes upfront chemotherapy, usually without biopsy, followed by nephrectomy, which must be performed rigorously, precisely and according to a protocol by the pathologist in order to classify the tumour into its appropriate risk group (low risk, intermediate risk or high risk) and to assess its local stage of extension (stage 1, 2 or 3). These criteria will determine the choice and duration of post-operative chemotherapy, with or without radiotherapy. The molecular abnormalities of nephroblastoma are heterogeneous, involving several chromosomal regions such as 1p, 16q, 1q, 11p15 and several genes such as WT1, CTNNB1, WTX, SIX1/2, DROSHA/DGCR8, TP53, MYCN, FBXW7 and TRIM28. Analyses are underway to determine whether these molecular abnormalities associated with the absolute volume of chemoresistant blastema could help divide children into different groups. In 15% of cases, these are tumours other than nephroblastoma, very different from one another, with a highly variable prognosis ranging from benign tumours such as nephrogenic rest, paediatric cystic nephroma and metanephric tumour to very aggressive tumours such as rhabdoid tumour of the kidney or medullary carcinoma of the kidney. In this group, each tumour has its own genetics, whose molecular mechanisms are increasingly well understood, with fusions, tandem duplications or gene mutations which can help the pathologist to achieve to an accurate diagnosis in each morphological context. In some situations, the identification of these molecular alterations may lead to a targeted treatment. - Source: PubMed
Publication date: 2026/03/24
L'Herminé-Coulomb AuroreBerrebi Dominique