DDX48 antibody - middle region (ARP36422_T100)
- Known as:
- DDX48 (anti-) - middle region (ARP36422_T100)
- Catalog number:
- arp36422_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- DDX48 antibody - middle region (ARP36422_T100)
Ask about this productRelated genes to: DDX48 antibody - middle region (ARP36422_T100)
- Gene:
- EIF4A3 NIH gene
- Name:
- eukaryotic translation initiation factor 4A3
- Previous symbol:
- DDX48
- Synonyms:
- KIAA0111, EIF4AIII, Fal1
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2019-04-23
Related products to: DDX48 antibody - middle region (ARP36422_T100)
Related articles to: DDX48 antibody - middle region (ARP36422_T100)
- Environmental heavy metal exposure represents a well-established etiological factor in pulmonary carcinogenesis. Although ferroptosis dysregulation contributes to Cadmium (Cd) induced pulmonary carcinogenesis, its precise molecular determinants remain elusive. Here, we demonstrated that Cd treatment (5 μM) induced EIF4A3-mediated downregulation of circ_0073586 in human bronchial epithelial (16HBE) cells, which functionally promoted malignant transformation. Intriguingly, we observed that ferroptosis was markedly suppressed in malignant transformed cells as the exposure duration increased, a suppression that was significantly reversed by circ_0073586 overexpression. Mechanistically, circ_0073586 acted as a molecular decoy for the RNA-binding protein SRSF9, thereby effectively suppressing GPX4-dependent cellular ferroptosis through the Wnt/β-catenin pathway. These findings were validated in vivo, where Cd-exposed murine models at 36 weeks exhibited concurrent downregulation of circ_0073586 and suppression of ferroptosis, with these changes showing a strong correlation. Thus, the study not noly reveals a critical crosstalk between metabolism-associated cell death and epigenetic regulation during Cd-induced pulmonary carcinogenesis, but also identifies potential molecular targets for intervention in heavy metal-associated lung cancer. - Source: PubMed
Publication date: 2026/08/25
Wang DongleiWang WenyuShao YueqingLi YanshuWang YaliLi BingyunHuang Lihua - Cervical cancer is a common gynecological malignancy, having high incidence and mortality rates, especially in developing regions. The tumor microenvironment (TME) plays a crucial role in disease progression, and cancer-associated fibroblasts (CAFs) are key components of the TME. However, the roles of CAFs in tumor-adjacent normal tissue remain unclear. - Source: PubMed
Publication date: 2026/08/10
Liu YiYin DinglingWu LuWang HuanSong YijunHuang JieZhou JiaxiongLi HaoxianLiang PeiliFeng JinghuiHe Hong - Despite the importance of exon junction complexes (EJCs) to co- and post-transcriptional gene control, how and when the EJC core of EIF4A3, RBM8A, and MAGOH, and the peripheral factors of the alternative RNPS1-EJC and CASC3-EJC, assemble on spliceosomes remain unclear. Existing characterizations that order EJC assembly on spliceosomes offer different conclusions. Using immunoprecipitations (IPs) of EIF4A3, RNPS1, or CASC3 in the presence of RNase I followed by liquid chromatography followed by tandem mass spectrometry (LC-MS/MS) analyses of human HEK293T cells, we expand upon those splicing factors that associate with EJC constituents. Referencing these data against existing cryogenic electron microscopy (cryo-EM) spliceosome structures at different stages of pre-messenger RNA (pre-mRNA) splicing, coupled with data from a series of western blots of nuclear fractions before and after IP, we report that EIF4A3, RBM8A, MAGOH, and RNPS1 associate with assembled but inactive spliceosomes. This is followed by CASC3 joining to late activated spliceosomes. Our work bridges long-standing gaps in understanding EJC assembly on spliceosomes. - Source: PubMed
Abshire Elizabeth TMaquat Lynne E - High altitude (HA) is associated with environmental stress and low oxygen levels, and HA adaptation varies among populations. This study aimed to explore HA adaptation-related circular RNAs (circRNAs) and their transcriptomic profiles. We performed high-throughput analysis on male individuals from three populations at different altitudes and identified gene copy number variations (CNVs) and numerous differentially expressed circRNAs (DEcircRNAs) via pairwise comparisons. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses showed that the parent genes of DEcircRNAs were enriched in biological regulation and the hypoxia-inducible factor-1 (HIF-1) signaling pathway. Five key DEcircRNAs (hsa_circ_0044526, hsa_circ_0022498, hsa_circ_0044534, hsa_circ_0044520, and hsa_circ_0026102) interacting with RBPs (argonaute 2 protein (AGO2) and eukaryotic translation initiation factor 4A3 (EIF4A3)) were identified. Their expression increased with altitude, with the highest expression observed at 3,000 m). Overexpression of HIF-1 was positively correlated with the upregulated expression of the five circRNAs in human endothelial cells, offering preliminary correlative evidence for investigating hypoxia-associated transcriptional links underlying high-altitude adaptation. Collectively, these DEcircRNAs may contribute to HIF-1-mediated HA adaptive metabolism. - Source: PubMed
Publication date: 2026/08/10
Bao BuheYu MingxuanPang WeiWang RuilinDong WenbinBai YingShi RuiWang Renjie - The contribution of post-transcriptional regulation remains largely unexplored in thyrotropin-secreting pituitary tumors (TSHomas), a rare endocrine pathology responsible for inappropriate TSH secretion and central hyperthyroidism. We investigated the TSHoma post-transcriptional regulatory landscape by analyzing components of molecular machineries controlling RNA metabolism [spliceosome/RNA-exosome/nonsense-mediated decay (NMD)], their associations with clinical parameters, and the impact of their pharmacological inhibition in TSHoma cells. A drastic dysregulation of multiple components of spliceosome [spliceosome (/) and splicing factors (e.g., // …)], RNA-Exosome (e.g., //), and NMD [e.g., , and NMD-canonical targets (/)] was found in TSHomas vs. non-tumor pituitaries with some of these alterations associated with relevant clinical features (e.g., tumor size, TSHB/fT4-levels). Moreover, we demonstrate a clear antiproliferative action of spliceosome/RNA-Exosome/NMD inhibitors in primary patient-derived TSHoma cells. Overall, a clinically relevant spliceosome/RNA-Exosome/NMD-associated molecular dysregulation and antiproliferative actions of these machineries' inhibition are demonstrated in TSHomas, highlighting a potential source of novel diagnostic/prognostic biomarkers and therapeutic tools in TSHomas. - Source: PubMed
Publication date: 2026/08/06
G-García Miguel EFlores-Martínez ÁlvaroArroyo-Millán LauraVenegas EvaDiaz-Perdigones Cristina MMaraver SilviaCano DavidArráez CintaArráez Miguel AJapón Miguel AMartínez-Fuentes Antonio JSoto-Moreno AlfonsoFuentes-Fayos Antonio CHerrera-Martínez Aura DLuque Raúl M