Ask about this productRelated genes to: RIOK3 Blocking Peptide
- Gene:
- RIOK3 NIH gene
- Name:
- RIO kinase 3
- Previous symbol:
- SUDD
- Synonyms:
- -
- Chromosome:
- 18q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-01
- Date modifiied:
- 2019-03-15
Related products to: RIOK3 Blocking Peptide
Related articles to: RIOK3 Blocking Peptide
- The incidence of prostate cancer continues to increase, making it the second most common malignant tumor among men worldwide. Immunotherapy has emerged as a key therapeutic strategy for treating tumors. Numerous studies have established that the efficacy of tumor immunotherapy is closely associated with the tumor microenvironment and T cell subsets. However, the specific functions of certain T cell subsets in prostate cancer remain incompletely characterized. Therefore, this study aimed to systematically investigate the distribution patterns of T cell subsets within the tumor microenvironment of prostate cancer patients and their correlations with clinicopathological parameters. Therefore, we investigated the impact of T cells on the tumor microenvironment of prostate cancer at the single-cell level. We employed a variety of analytical methods to reveal the functions of T cells, including cell interaction analysis, time-series analysis, enrichment analysis, immune infiltration analysis, and other analytical approaches. By integrating bulk RNA-seq data, we constructed and validated a prognostic risk model based on T cell marker genes. Finally, we utilized the ssGSEA and ESTIMATE algorithms to explore the relationship between the prognostic risk model and immunotherapy. After quality control, 16,999 cells from the single-cell data were retained for downstream analysis. Our study focused on T cells, revealing the communication between various cell types and T cells. Pseudotime analysis showed that different T cell marker genes exhibited differential expression at various time points, corresponding to distinct biological processes. Enrichment analysis indicated that T cell marker genes were enriched in several immune-related pathways. From our analysis, BCAS2, EIF2S2, RIOK3, and ATP6V1E1 were ultimately identified as prognostic markers. Immune infiltration analysis revealed that high-risk patients had lower immune scores, stromal scores, and ESTIMATE scores and greater tumor purity compared to low-risk patients. We analyzed the mechanisms involving T cells in prostate cancer from multiple perspectives, constructed a prognostic model, and conducted immune infiltration analysis. Our findings contribute to the understanding of prostate cancer and its prognosis, providing valuable insights for future research and prognostic assessments in prostate cancer. - Source: PubMed
Publication date: 2025/12/31
Wang ZhiduXing YanShang DongmeiJin Xuefei - Neuroblastoma (NB), a pediatric solid malignancy, is distinguished by hetergenous clinical characteristics, including tumor aggressiveness or spontaneous regression. Nevertheless, the regulatory mechanisms and therapeutic approaches underlying these processes are still mainly unknown. Herein, RAR-related orphan receptor B (RORB) as a transcription factor repressing nuclear factor kappa B (NF-κB) signaling involved in lysosomal biogenesis of NB. RORB attenuated the growth, invasiveness, and metastatic spread of NB cells are identified. From a mechanistic perspective, RORB increased the transcription of nuclear receptor subfamily 1 group D member 1 (NR1D1)- or RIO kinase 3 (RIOK3)- in a circadian clock-dependent manner, resulting in suppression of NF-κB activity, subsequent derepression of folliculin (FLCN)- or folliculin interacting protein 1 (FNIP1)- levels, and decrease of lysosomal biogenesis in NB cells. Meanwhile, in liquid condensates, RNA binding motif protein 10 (RBM10) interacted with RORB to repress its transactivation and exerted oncogenic roles in lysosomal biogenesis and aggressiveness of NB cells. Pre-clinically, a small peptide is able to block the interaction between RBM10 and RORB, and suppresses lysosomal biogenesis, tumorigenesis, and aggressiveness. High levels of RORB, NR1D1, RIOK3, FLCN, and FNIP1, or low expression of RBM10, are linked to favorable prognosis of clinical NB cases. These results indicate that targeting RBM10-repressed RORB activity in liquid condensates inhibits lysosomal biogenesis and NB progression via affecting NF-κB signaling. - Source: PubMed
Publication date: 2025/09/03
Guo YanhuaWang XiaojingYang ChunhuiWang ZhijieWang XiaolinLi XinyueQu JiayingZhou ShunchenZheng LiduanTong Qiangsong - Respiratory Syncytial Virus (RSV) is a leading cause of lower respiratory tract infections, particularly in vulnerable populations such as infants, the elderly, and immunocompromised individuals. RSV infection can result in mortality rates as high as 20%, attributable not only to viral replication but also to an excessive host immune response. Current therapeutic options are limited, partly due to gaps in understanding the host immune response, especially the role of macrophages and their signaling pathways. This study investigates the role of RIOK3, an unconventional kinase, in modulating the Jak1/STAT1 pathway during RSV infection in macrophages and its impact on viral replication and interferon production. Using both and models, including primary bone marrow-derived macrophages (BMM) from control and RIOK3 knockout (KO) mice, we demonstrate that RIOK3 is a critical regulator of the Jak1/STAT1 pathway in macrophages during RSV infection. The absence of RIOK3 enhances viral replication and disrupts the balance of type I interferons. Targeting RIOK3 may represent a promising strategy to enhance antiviral immunity and mitigate RSV-induced inflammation, thus warranting further investigation for therapeutic potential. - Source: PubMed
Publication date: 2025/04/30
Sun FangfangLiang WeiweiQian YingyingHu Pengfei - Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies with few effective therapies available. We previously determined the essential role of Zic family member 5 (ZIC5) in the survival of PDAC cells. In this study, we showed that targeting ZIC5 can effectively shrink PDAC tumors treated with gemcitabine in vivo and investigated the molecular mechanisms involved. When tumor-bearing mice were injected intravenously with ZIC5-targeting small interfering RNA, tumor volume was significantly reduced by gemcitabine treatment. RNA-sequencing analysis was used to identify the genes affected by ZIC5 knockdown. Among these, we selected the genes whose mRNA expression levels correlated with that of ZIC5 in pancreatic cancer and those associated with poor prognosis in patients with pancreatic cancer. Further analysis revealed that RIO kinase 3 (RIOK3) promotes PDAC cell survival, whereas ALDH3B1, PTGES, and TUFT1 contribute to gemcitabine resistance in MiaPaca-2 cells. We identified RIOK3 as a direct target gene of ZIC5 using ChIP and luciferase assays. Furthermore, stable expression of RIOK3 in PANC-1 cells reversed the reduction in cell number following ZIC5 knockdown. These findings highlight RIOK3 as a critical target of ZIC5, which is involved in survival signaling in PDAC cells. - Source: PubMed
Publication date: 2025/05/03
Satow ReikoKashiwaba YukiOkao MisakiTakano ShinAiga YunaYoneda AtsukoHosomichi KazuyoshiFukami Kiyoko - The initiation-specific ribosome-associated quality control pathway (iRQC) is activated when translation initiation complexes fail to transition to elongation-competent 80S ribosomes. Upon iRQC activation, RNF10 ubiquitylates the 40S proteins uS3 and uS5, which leads to 40S decay. How iRQC is activated in the absence of pharmacological translation inhibitors and what mechanisms govern iRQC capacity and activity remain unanswered questions. Here, we demonstrate that altering 60S:40S stoichiometry by disrupting 60S biogenesis triggers iRQC activation and 40S decay. Depleting the critical scanning helicase eIF4A1 impairs 40S ubiquitylation and degradation, indicating mRNA engagement is required for iRQC. We show that amino acid starvation conditions also stimulate iRQC-dependent 40S decay. We identify RIOK3 as a crucial iRQC factor that interacts with ubiquitylated 40S subunits to mediate degradation. Both RNF10 and RIOK3 protein levels increase upon iRQC pathway activation, establishing a feedforward mechanism that regulates iRQC capacity and subsequent 40S decay. - Source: PubMed
Publication date: 2025/02/28
Ford Pierce WGarshott Danielle MNarasimhan MythreyiGe XuezhenJordahl Eric MSubramanya ShubhaBennett Eric J