h RIOK3 inducible lentiviral particles
- Known as:
- h RIOK3 inducible lentiviral beads
- Catalog number:
- LVP251
- Product Quantity:
- 1x107 IFU/ml x 200ul
- Category:
- -
- Supplier:
- GenTarget
- Gene target:
- RIOK3 inducible lentiviral particles
Related genes to: h RIOK3 inducible lentiviral particles
- 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: h RIOK3 inducible lentiviral particles
136 kDa double-stranded RNA-binding protein,ADAR,ADAR1,Double-stranded RNA-specific adenosine deaminase,DRADA,DSRAD,G1P1,Homo sapiens,Human,IFI4,IFI-4,Interferon-inducible protein 4,K88DSRBP,p13615-oxoprostaglandin 13-reductase,D3T-inducible gene 1 protein,Dig1,DIG-1,Dithiolethione-inducible gene 1 protein,Ltb4dh,NADP-dependent leukotriene B4 12-hydroxydehydrogenase,PRG-1,Prostaglandin reduct15E1.1,Homo sapiens,HSPC132,Human,p53CSV,p53-inducible cell-survival factor,Protein 15E1.1,TP53-regulated inhibitor of apoptosis 1,TRIAP1,WF-115e1.1,Mouse,Mus musculus,p53CSV,p53-inducible cell-survival factor,Protein 15E1.1,TP53-regulated inhibitor of apoptosis 1,Triap1,WF-13-keto acyl-CoA synthase Elovl3,Cig30,CIN-2,Cold-inducible glycoprotein of 30 kDa,Elongation of very long chain fatty acids protein 3,Elovl3,Mouse,Mus musculus3-keto acyl-CoA synthase ELOVL3,CIG30,Cold-inducible glycoprotein of 30 kDa,Elongation of very long chain fatty acids protein 3,ELOVL3,Homo sapiens,Human33,ERBB receptor feedback inhibitor 1,Errfi1,Gene 33 polypeptide,Mig6,MIG-6,Mitogen-inducible gene 6 protein homolog,RALT,Rat,Rattus norvegicus,Receptor-associated late transducer6Ckine,Beta-chemokine exodus-2,C-C motif chemokine 21b,Ccl21b,Mouse,Mus musculus,Scya21,Scya21b,Small-inducible cytokine A21b,TCA4,Thymus-derived chemotactic agent 46Ckine,Beta-chemokine exodus-2,C-C motif chemokine 21c,Ccl21c,Mouse,Mus musculus,Scya21c,Small-inducible cytokine A21c,TCA4,Thymus-derived chemotactic agent 4A18 hnRNP,A18HNRNP,CIRBP,CIRP,Cold-inducible RNA-binding protein,Glycine-rich RNA-binding protein CIRP,Homo sapiens,HumanA18 hnRNP,Cirbp,Cirp,Cold-inducible RNA-binding protein,Glycine-rich RNA-binding protein CIRP,Mouse,Mus musculusA18 hnRNP,Cirbp,Cirp,Cold-inducible RNA-binding protein,Glycine-rich RNA-binding protein CIRP,Rat,Rattus norvegicusAccuCount Blank Particles, 106_mL, 13.0-17.9 μm, 10 mLAccuCount Blank Particles, 106_mL, 2.0-2.4 μm, 10 mLAccuCount Blank Particles, 106_mL, 5.0-5.9 μm, 10 mL Related articles to: h RIOK3 inducible lentiviral particles
- Stresses like starvation trigger degradation of mature 40S ribosomes, requiring the coordinated breakdown of large and stable RNA-protein complexes. The atypical kinase RIOK3 orchestrates degradation by binding ubiquitylated 40S ribosomes and promoting rRNA decay. However, the mechanisms and factors that mediate rRNA decay remain unknown. Here we find that in response to starvation, RIOK3 recruits the terminal uridylyl-transferase TUT7 and the exonuclease DIS3L2 to 40S ribosomes. Sequencing analyses show that TUT7 adds oligo(uridine) tails to the 3' end of the 18S rRNA in these ribosomes. DIS3L2 subsequently recognizes uridylated 18S rRNA and carries out 3'-5' decay. We identify major decay intermediates that undergo further uridylation in a process of iterative uridylation and decay. Loss of DIS3L2 impairs 18S rRNA decay during starvation and leads to accumulation of uridylated 18S rRNA. Together these findings define a mechanism for ribosome degradation in which 3' oligo(uridine) tailing drives decay of rRNA from ribosomes. - Source: PubMed
Publication date: 2026/04/27
Diehl Frances FBuskirk Allen RGreen Rachel - 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