Human Interleukin 24,IL-24 ELISA KIT
- Known as:
- Human Interleukin 24,Interleukin-24 Enzyme-linked immunosorbent assay test KIT
- Catalog number:
- 201-12-2163
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 24 IL-24 ELISA KIT
Related genes to: Human Interleukin 24,IL-24 ELISA KIT
- Gene:
- IL24 NIH gene
- Name:
- interleukin 24
- Previous symbol:
- ST16
- Synonyms:
- mda-7, IL10B, Mob-5, C49A, FISP, IL-24
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-02
- Date modifiied:
- 2016-10-05
Related products to: Human Interleukin 24,IL-24 ELISA KIT
Related articles to: Human Interleukin 24,IL-24 ELISA KIT
- Dengue virus (DENV) infection has emerged as a critical global public health challenge, particularly in tropical and subtropical regions, where it continues to cause high morbidity rates and severe disease risks. Given the current lack of specific antiviral therapies in clinical practice, the development of novel anti-DENV agents represents an urgent medical need. In this study, the antiviral activity of a novel compound, TXD-174, was systematically evaluated. It was found that TXD-174 exhibited significant inhibitory effects against DENV2 in vitro. Notably, viral replication was effectively blocked by TXD-174, while cytotoxicity assessments revealed a favorable therapeutic window. Furthermore, the compound demonstrated inhibitory activity against all four DENV serotypes, highlighting its potential as a broad-spectrum anti-dengue agent. Meanwhile, RNA-seq analysis indicated that level of IL-24 was significantly upregulated. Knockdown of IL-24 gene reduced the antiviral effect of TXD-174, while overexpression of IL-24 gene also exhibited good antiviral effects. In virus-infected AG-129 models, TXD-174 was also found to have good in vivo antiviral effects. These findings establish a foundation for further exploration of targeted therapeutic strategies against DENV infections. - Source: PubMed
Han JiajiaKong WeiyaGuo DanLiu ShuwenTang XiaodongYao Xingang - Plasma inflammatory protein biomarkers associated with clinical milestone heterogeneity in Parkinson's disease (PD) remain undefined. We measured 92 inflammation-related plasma proteins in 82 PD patients using the Olink Proximity Extension Assay. No proteins differed significantly between fallers and non-fallers. However, among fallers, plasma interleukin-24 showed the strongest correlation with observed time to first fall (unadjusted r = 0.752, q = 0.071), and this signal was also observed in an exploratory covariate-adjusted model (q = 0.030). Colony-stimulating factor 1 showed a comparable but non-significant correlation. In group comparisons for symptomatic orthostatic hypotension, CCL11 differed significantly between patients with and without symptomatic orthostatic hypotension (q = 0.0004). These exploratory findings highlight candidate inflammatory protein profiles related to milestone heterogeneity in PD, warranting validation in longitudinal cohorts. - Source: PubMed
Publication date: 2026/07/31
Iwaoka KazuhiroTaguchi KeitaOikawa SayuriToyoshiba HiroyoshiAndo TatsuyaMaeda Tetsuya - Traditional Chinese medicines are based on complex mixtures of natural products and their multi-target mechanism of action. Therefore the discovery and validation of targets and mechanisms have always been challenging. In previous studies, using transcriptomic methods and Compound Kushen Injection (CKI) as a model drug, we identified multiple pathways and candidate target genes for validation, through which CKI exerts its pharmacological effects. - Source: PubMed
Publication date: 2026/07/16
Shen HanyuanNourmohammadi SaeedZhou YanHarata-Lee YukaQu ZhipengWang WeiYool Andrea JAdelson David L - Oxaliplatin-based chemotherapy is a principal treatment for colon cancer, but drug resistance hinders its efficacy. Cancer cell dormancy is reportedly a crucial driver of chemoresistance. IL-24 functions vitally in tumor chemoresistance, yet its role in colon cancer dormancy and oxaliplatin resistance remains unexplored.IL-24 expression was assessed in colon cancer tissues and cells via RT-qPCR, western blotting, or immunohistochemistry. The functions of IL-24 in colon cancer cell proliferation, apoptosis, dormancy, and oxaliplatin resistance were evaluated by CCK-8, flow cytometry, and western blotting. The downstream mechanism of IL-24 was predicted using RNA sequencing and bioinformatics analyses and verified in vitro. A tumor xenograft mouse model was built to further verify the role of IL-24 in colon cancer. IL-24 was overexpressed in oxaliplatin-resistant colon cancer tissues and cells. Furthermore, IL-24 treatment reversed the anti-proliferative and pro-apoptotic effects of oxaliplatin on colon cancer cells. Regarding cell dormancy, IL-24 treatment triggered G0/G1 cell cycle arrest and upregulated dormancy markers (CDKN1A, CDKN1B, TGFB2, and MSK1). Bioinformatics analyses revealed that IL-24 might function in colon cancer mainly through NF-κB pathway, and IL-24 activated the NF-κB axis in tumor cells. Importantly, treatment with NF-κB inhibitor reversed IL-24-induced colon cancer cell dormancy and oxaliplatin resistance. In vivo, IL-24 treatment abolished the anti-tumor effects of oxaliplatin, promoted cell dormancy, and activated NF-κB signaling in tumor tissues. IL-24 induces colon cancer cell dormancy and oxaliplatin resistance by activating NF-κB signaling. The IL-24/NF-κB axis may serve as a likely target to alleviate oxaliplatin resistance in colon cancer. - Source: PubMed
Publication date: 2026/07/16
Hu YanyanLi ShengyingZhu MinjingGong ChaojuFang Zejun - Crohn's disease (CD) is a chronic inflammatory condition of the gastrointestinal tract, where oxidative stress is a significant contributing factor to its pathogenesis. This study utilized multi-omics data, including RNA sequencing from the GSE216447 dataset and three genome-wide association studies (GWAS) datasets (ieu-a-10, ieu-a-11, ieu-a-13), to investigate the molecular networks related to oxidative stress in CD. Differential expression analysis was performed using DESeq2, followed by pathway enrichment analysis with clusterProfiler. Protein-protein interaction (PPI) networks were constructed using the STRING database. Mendelian Randomization (MR) analysis was conducted using TwoSampleMR and MRMix to identify causal relationships between genetic variants and CD. Quantitative real-time polymerase chain reaction (qPCR) was further applied to verify key differentially expressed genes (DEGs), including FASN, HMGCR, ASCC3, CD101, ELOVL6, PHLDA2, PHLDA3, and SCPEP1, in intestinal mucosal samples from both inactive and active CD patients. The analysis identified 64 up-regulated and 46 down-regulated differentially expressed genes (DEGs) in response to HO intervention. Key pathways related to oxidative stress, including the p53 signalling pathway and steroid biosynthesis, were significantly enriched. Consistent with transcriptomic data, qPCR confirmed that FASN and HMGCR were significantly upregulated in inactive CD, while ASCC3, CD101, ELOVL6, PHLDA2, PHLDA3, and SCPEP1 were markedly increased in active CD (all p < 0.05). The MR analysis revealed that in the dataset ieu-a-10, ABCB9 and OSGIN1 were identified as having a significant causal relationship with CD using TwoSampleMR, while only OSGIN1 was significant in MRMix. In dataset ieu-a-11, ARL4C, CD101, HMGCR, and IL24 were found to be significantly associated with CD, with overlapping findings between TwoSampleMR and MRMix. For dataset ieu-a-13, ACTA2 and CD101 were consistently identified as significant, suggesting their potential roles in CD pathogenesis. The findings highlight the crucial involvement of oxidative stress-related molecular networks in CD and underscore the utility of Mendelian Randomization in elucidating causal genetic factors. qPCR validation confirmed persistent upregulation of lipid metabolism genes in inactive CD and significant elevation of inflammation-related genes in active CD, reinforcing the link between oxidative stress and disease activity. - Source: PubMed
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