Polyclonal Rabbit DDX24 Antibody
- Known as:
- Polyclonal Rabbit DDX24 Antibody
- Catalog number:
- KA1035
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit DDX24 Antibody
Related genes to: Polyclonal Rabbit DDX24 Antibody
- Gene:
- DDX24 NIH gene
- Name:
- DEAD-box helicase 24
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q32.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-19
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit DDX24 Antibody
Related articles to: Polyclonal Rabbit DDX24 Antibody
- Ovarian cancer (OC) remains a major cause of gynecologic cancer mortality, with progress in targeted therapy limited by an incomplete understanding of post-transcriptional oncogenic drivers. Dysregulated RNA splicing-particularly intron retention (IR)-is increasingly recognized as a key driver of tumor progression. Here, integrated transcriptomic and proteomic analyses identify SNRPF, a core spliceosomal component, as a potent oncogenic driver in OC. SNRPF is highly expressed in tumor specimens, and its overexpression predicts poor patient survival. Silencing SNRPF suppresses proliferation, invasion, and xenograft growth. IR-focused analysis reveals that SNRPF depletion induces intron 6 retention in DDX24, disrupting the Helicase_C domain and generating premature termination codons that activate nonsense-mediated decay (NMD), thereby reducing DDX24 protein abundance and markedly impairing its oncogenic function. DDX24 depletion similarly promotes intron 2 retention in E2F4, causing NMD-mediated downregulation. Notably, E2F4 directly binds the SNRPF promoter, forming a self-sustaining "SNRPF-DDX24-E2F4" axis linking splicing and transcriptional regulation. Antisense oligonucleotide-mediated inhibition of SNRPF disrupts this feedback loop, downregulates DDX24 and E2F4 via IR, and significantly impairs tumor growth in vitro, in vivo, and in patient-derived xenografts. These findings define a splicing-transcription coupling mechanism in OC and position SNRPF as a promising therapeutic target. - Source: PubMed
Publication date: 2026/05/10
Li YingweiChen ZhongshaoGao QianqianGao YuehanYang Ning - - Source: PubMed
Publication date: 2026/04/09
Shen XingkaiJin YangliYang KailiQian XinyeGuo Jian - Sepsis is a systemic inflammatory response syndrome caused by an infection featuring high morbidity and mortality due to complex mechanisms underlying immune dysfunction. In this study, based on the sepsis transcriptome profiles from the GEO datasets (GSE65682, GSE28750, GSE95233, and GSE167363), we used the machine learning method and other computational algorithms, such as differential gene expression analysis, weighted gene coexpression network analyses (WGCNA), and the building of PPI networks to identify four hub genes (DDX24, GZMM, KCNA3, and NCL). The quantitative reverse transcription PCR performed preliminary validation that all four hub genes were significantly downregulated in patients with sepsis. DDX24 had the highest diagnostic performance (AUC > 0.8) for discriminating patients from normal subjects. GZMM was found to be significantly related to the prognoses of patients as well as APACHE II scores, and the downregulated expression pattern might represent T cell and NK cell exhaustion. Analysis based on single-cell RNA sequencing showed that DDX24 and GZMM were mainly expressed in T cells and NK cells, and the expression trends strongly correlate with patient survival. Functional enrichment analysis suggested that the hub genes likely participate in regulation of immune responses, especially those pertaining to T cells. Drug prediction found 25 candidate drugs that will serve as new therapeutic targets for precision medicine to treat sepsis. Overall, the multifaceted study shed light on key roles played by these hub genes (especially DDX24 and GZMM) in the development of sepsis and will be useful references in diagnosing patients and estimating prognosis. - Source: PubMed
Publication date: 2026/04/03
Zhang YiTang LiangWu JuanYang LinLiu WenLiang YiHan JianfangHe ShuangYang Yulian - DEAD-box (DDX) RNA helicases play critical roles in gene regulation by interacting with RNAs and influencing RNA fate and function. Our previous study associated DDX24 dysfunction with vascular development, but its precise role in RNA metabolism in the context of angiogenesis remains unclear. Here, we identified DDX24-bound messenger RNAs (mRNAs) in endothelial cells using infrared cross-linking immunoprecipitation sequencing. We found that DDX24 modulates endothelial cell functions by directly binding to and regulating specific mRNA targets that are crucial for vascular development and angiogenesis, such as CLEC14A and ERG. Mechanistically, DDX24 promotes the decay of these mRNA targets in a CCR4-NOT deadenylase complex-dependent manner. These results establish a link between DDX24-dependent regulation of mRNA stability and endothelial cell function, providing novel therapeutic targets for angiogenesis-related diseases. - Source: PubMed
He SimengLi BinChen FangbinHuang JunhongDong YingyingLiu ShurongLiu ChangZhang QianqianWang LijieShan HongGong YujiaoYang JianhuaHe Huanhuan - The blood-brain barrier (BBB) is essential for brain function, yet its underlying regulatory mechanisms remain elusive. Here, we identify DEAD-box RNA helicase 24 (DDX24) as a regulator of the BBB. Endothelial-specific Ddx24 knockout (Ddx24) mice exhibit deficits in learning and memory and increased BBB permeability. Furthermore, DDX24 knockdown in human cerebral microvascular endothelial cells (hCMEC/D3) disrupts the barrier function through occludin phosphorylation and mitochondrial dysfunction. Targeting NADPH oxidase suppresses BBB hyperpermeability and improves learning and memory deficits in Ddx24 mice. Mechanistically, the DDX24 protein binds to PPFIA4 mRNA and enhances its stability. Consistent with the function of DDX24, PPFIA4 knockdown impairs mitochondrial homeostasis and barrier function in hCMEC/D3 cells. Importantly, DDX24 overexpression attenuates Aβ-induced barrier damage. Taken together, our study uncovers a pivotal role for DDX24 in regulating the BBB via mediating mitochondrial function in endothelial cells, providing a potential therapeutic target for treating BBB-related diseases. - Source: PubMed
Publication date: 2025/10/15
Li ShuaiLiu YuxuanDong YingyingGong YujiaoHe SimengYuan JianyuDeng ShengfengZhang QianqianWang LijieLiu FeiTu QiuyunShan HongHe Huanhuan