DDX31 antibody - N-terminal region (ARP36491_T100)
- Known as:
- DDX31 (anti-) - N-terminal region (ARP36491_T100)
- Catalog number:
- arp36491_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- DDX31 antibody - N-terminal region (ARP36491_T100)
Related genes to: DDX31 antibody - N-terminal region (ARP36491_T100)
- Gene:
- DDX31 NIH gene
- Name:
- DEAD-box helicase 31
- Previous symbol:
- -
- Synonyms:
- FLJ13633, FLJ23349, FLJ14578, PPP1R25
- Chromosome:
- 9q34.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-27
- Date modifiied:
- 2016-10-05
Related products to: DDX31 antibody - N-terminal region (ARP36491_T100)
Related articles to: DDX31 antibody - N-terminal region (ARP36491_T100)
- The nonsense-mediated messenger RNA decay (NMD) surveillance system detects and selectively eliminates transcripts with premature stop codons. A stop codon is considered premature if it is followed by an exon-exon junction >50 nucleotides downstream. Pruning of the 3'-untranslated region containing such junctions through alternative polyadenylation may provide a mechanism of NMD escape. Here, we systematically examine a subclass of poison exons that carry a premature stop codon for the presence of polyadenylation sites (PAS) in the downstream intron. Using data from the GTEx consortium, we observed that poison exons are more often followed by an active polyadenylation site compared with cassette exons. We also identified tissue-specific switches between NMD-targeted and NMD-escape isoforms in several human genes, including the vaccinia-related kinase , nuclear transcription factor , Notch pathway regulator , and RNA helicase . Blocking the cleavage and PAS in these genes using antisense oligonucleotides in human cells led to a switch from NMD-escape to NMD-target isoform, accompanied by a decrease in gene expression levels. This study reveals that NMD escape via alternative polyadenylation is a widespread, yet currently overlooked post-transcriptional mechanism of gene expression regulation. - Source: PubMed
Publication date: 2026/05/20
Vlasenok MariaKuznetsova AntoninaSkvortsov Dmitry ADontsova Olga APervouchine Dmitri D - Head and neck squamous cell carcinoma (HNSCC) has great aggressiveness and a high early lymph node metastasis rate. Ribosome biogenesis (RiBi) is frequently hyperactivated in tumors and is strongly associated with oncogenesis. However, its function in HNSCC lymph node metastasis is poorly characterized. Here, we found TBC1D14 expression was downregulated in lymph node-metastatic HNSCC and inversely correlated with Pol I expression. TBC1D14 suppressed RiBi in HNSCC by bioinformatics mining and in vitro experiments. And inhibiting RiBi effectively reduced the proliferation, invasion, and migration capacities of HNSCC cells in vitro. In addition, inhibiting RiBi within TBC1D14-knockdown HNSCC cells suppressed epithelial-mesenchymal transition (EMT). Further in vivo experimentation substantiated that suppression of RiBi in HNSCC effectively attenuated TBC1D14 silencing-induced augmentation of tumor progression and lymph node metastasis. Analysis of our previous proteomic profiling data revealed that DDX31 was significantly downregulated in TBC1D14-overexpressing cells. Further investigations revealed that TBC1D14 inhibited RiBi by promoting the degradation of DDX31 via the ubiquitination pathway. Finally, we found that DDX31 underwent ubiquitination-dependent degradation via the TRIM25-mediated and K63-linked polyubiquitination pathway. Overall, our study demonstrates that TBC1D14 suppresses lymph node metastasis in HNSCC by promoting the ubiquitin-mediated degradation of DDX31 and subsequently inhibiting RiBi, consequently attenuating EMT. These findings revealed novel therapeutic targets for TBC1D14-deficient HNSCC. - Source: PubMed
Publication date: 2025/08/08
Liu YuhongWang MengnaLi YanshiLu TaoWang MinZhan WanyiChen LinHu GuohuaPan Min - Mis-sense mutations affecting TP53 promote carcinogenesis both by inactivating tumor suppression, and by conferring pro-carcinogenic activities. We report here that p53 DNA-binding domain (DBD) and transactivation domain (TAD) mis-sense mutants unexpectedly activate pro-carcinogenic epidermal growth factor receptor (EGFR) signaling via distinct, previously unrecognized molecular mechanisms. DBD- and TAD-specific TP53 mutants exhibited different cellular localization and induced distinct gene expression profiles. In multiple tissues, EGFR is stabilized by TAD and DBD mutants in the cytosolic and nuclear compartments respectively. TAD mutants promote EGFR-mediated signaling by enhancing EGFR interaction with AKT via DDX31 in the cytosol. Conversely, DBD mutants maintain EGFR activity in the nucleus, by blocking EGFR interaction with the phosphatase SHP1, triggering c-Myc and Cyclin D1 upregulation. Our findings suggest that p53 mutants carrying gain-of-function, mis-sense mutations affecting two different domains form new protein complexes that promote carcinogenesis by enhancing EGFR signaling via distinctive mechanisms, exposing clinically relevant therapeutic vulnerabilities. - Source: PubMed
Publication date: 2023/03/28
Ho Teresa Lai FongLee May YinGoh Hui ChinNg Germaine Yi NingLee Jane Jia HuiKannan SrinivasaraghavanLim Yan TingZhao TianyunLim Edwin Kok HaoPhua Cheryl Zi JinLee Yi FeiLim Rebecca Yi XuanNg Perry Jun HaoYuan JuChan Dedrick Kok HongLieske BettinaChong Choon SengLee Kuok ChungLum JeffreyCheong Wai KitYeoh Khay GuanTan Ker KanSobota Radoslaw MVerma Chandra SLane David PTam Wai LeongVenkitaraman Ashok R - VASA, also known as DDX4, is a member of the DEAD-box proteins and an RNA binding protein with an ATP-dependent RNA helicase. The VASA gene expression, which is required for human germ cell development, may lead to infertility. Immunocytochemistry and immunohistochemistry were used to examine the expression of VASA protein in the human testis sections of azoospermic patients, in-vitro and in-silico models. Some studies of fertile humans showed VASA expression in the basal and adluminal compartments of seminiferous tubules. Our Immunocytochemistry and immunohistochemistry in infertile humans showed expression of VASA in the luminal compartments of the seminiferous tubule. The immunohistochemical analysis of three human cases with different levels of non-obstructive azoospermia revealed a higher expression of VASA-positive cells. For this purpose, Enrichr and Shiny Gene Ontology databases were used for pathway enrichment analysis and gene ontology. STRING and Cytoscape online evaluation were applied to predict proteins' functional and molecular interactions and performed to recognize the master genes, respectively. According to the obtained results, the main molecular functions of the up-regulated and downregulated genes include the meiotic cell cycle, RNA binding, and differentiation. STRING and Cytoscape analyses presented seven genes, i.e., DDX5, TNP2, DDX3Y, TDRD6, SOHL2, DDX31, and SYCP3, as the hub genes involved in infertility with VASA co-function and protein-protein interaction. Our findings suggest that VASA and its interacting hub proteins could help determine the pathophysiology of germ cell abnormalities and infertility. - Source: PubMed
Publication date: 2022/10/14
Amirian MehdiAzizi HosseinHashemi Karoii DanialSkutella Thomas - Glioblastoma (GBM) is the most common brain tumor, with rapid proliferation and fatal invasiveness. Large-scale genetic and epigenetic profiling studies have identified targets among molecular subgroups, yet agents developed against these targets have failed in late clinical development. We obtained the genomic and clinical data of GBM patients from the Chinese Glioma Genome Atlas (CGGA) and performed the least absolute shrinkage and selection operator (LASSO) Cox analysis to establish a risk model incorporating 17 genes in the CGGA693 RNA-seq cohort. This risk model was successfully validated using the CGGA325 validation set. Based on Cox regression analysis, this risk model may be an independent indicator of clinical efficacy. We also developed a survival nomogram prediction model that combines the clinical features of OS. To determine the novel classification based on the risk model, we classified the patients into two clusters using ConsensusClusterPlus, and evaluated the tumor immune environment with ESTIMATE and CIBERSORT. We also constructed clinical traits-related and co-expression modules through WGCNA analysis. We identified eight genes (, and ) in the blue module and three genes (, , and ) in the turquoise module. Based on the public website TCGA, two biomarkers were significantly associated with poorer OS. Finally, through GSCALite, we re-evaluated the prognostic value of the essential biomarkers and verified as a hub biomarker. - Source: PubMed
Publication date: 2022/08/10
Jin YiWang ZhanwangXiang KaiminZhu YuxingCheng YaxinCao KeJiang Jiaode