RUVBL2 antibody - N-terminal region (ARP32378_T100)
- Known as:
- RUVBL2 (anti-) - N-terminal region (ARP32378_T100)
- Catalog number:
- arp32378_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RUVBL2 antibody - N-terminal region (ARP32378_T100)
Related genes to: RUVBL2 antibody - N-terminal region (ARP32378_T100)
- Gene:
- RUVBL2 NIH gene
- Name:
- RuvB like AAA ATPase 2
- Previous symbol:
- -
- Synonyms:
- RVB2, TIP48, TIP49b, Reptin52, ECP51, TIH2, INO80J, Rvb2
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2016-03-07
Related products to: RUVBL2 antibody - N-terminal region (ARP32378_T100)
Related articles to: RUVBL2 antibody - N-terminal region (ARP32378_T100)
- RuvB-like 1 (RUVBL1) and RuvB-like 2 (RUVBL2) are AAA ATPases that form hetero-oligomeric complexes involved in diverse cellular functions. Increasing evidence implicates the RUVBL1/2 complex as an essential cofactor of MYC, with RUVBL1/2 inhibition reducing c-MYC levels in vitro. Herein, we report a potent RUVBL1/2 inhibitor discovered through a Single-Molecule Tracking (SMT)-driven SAR campaign. Compared with a biochemical ADP-Glo assay, which exhibited limited dynamic range and poor reproducibility under our experimental conditions, the live-cell high-throughput RUVBL SMT assay provided robust and reproducible potency measurements and correlated strongly with cell viability and MYC degradation. Multiparameter optimization yielded compound 18, which demonstrated improved efficacy in a MYC-dependent Burkitt lymphoma xenograft model at a significantly lower dose than the RUVBL1/2 inhibitor CB-6644. This work establishes SMT as a powerful tool to facilitate the drug discovery SAR campaigns and evaluates the therapeutic potential of RUVBL1/2 inhibition in MYC-dependent cancers. - Source: PubMed
Publication date: 2026/04/22
Zheng LiPark EugeneLenihan JasonForrest William S RZhou XinFong CharmaineTang YangzhongKelly Marcus PDriouchi AmineTabatabaei AliWong HelenVargas Jesse DAlbright Samuel THoward ZacharySilva Maité BElliott Liam AFarley MichaelOrtega JoséJones StephenChang XiaoHeuer TaylorZheng QuanMorrison Huntly MBracho DanielDu QianLe JenniferTarafder AbhijitNawrocki GrzegorzSchyman PatricAkella LakshmiNguyen Mai KDing DaisyTao ArnoldPérez Fernando RodríguezVanBuren KaylaMalik RohitDumble MelissaAnderson Daniel JCleary LeahPiotrowski David WBeck Hilary P - The functional versatility of Hsp90 relies on its association with specialized co-chaperones that regulate client recruitment and maturation. Among these, the R2TP complex, comprising RUVBL1, RUVBL2, RPAP3 (Tah1 in yeast), and PIH1D1, acts as a conserved assembly factor essential for the biogenesis of large multiprotein machineries, including RNA polymerases, snoRNPs, PIKKs, and mTOR signaling complexes. RPAP3 functions as a central scaffold within the R2TP-Hsp90 system, linking Hsp90 and Hsp70 to the RUVBL1/2 ATPase core through its TPR domains and C-terminal interaction with PIH1D1. This modular organization enables RPAP3 to integrate chaperone-mediated folding with client delivery and complex assembly. Notably, dysregulation of RPAP3 has been implicated in oncogenic processes, highlighting its biomedical relevance. This review synthesizes current structural, functional, and evolutionary insights into RPAP3, focusing on its role within the R2TP-Hsp90 machinery and its emerging connections to human disease. - Source: PubMed
Publication date: 2026/04/09
Antonio Larissa MRamos Carlos H I - High-risk neuroblastoma is characterized by amplification and high or gene expression. These patients have a poor prognosis and there is an urgent need for more effective drugs. While strategies to develop inhibitors that directly target the MYC proteins have remained largely unsuccessful, recent preclinical studies have identified ATR, a key protein of the DNA damage response, as a promising alternative therapeutic target. Here, we identified a strong RUVBL1 and RUVBL2 signature in transcriptomics data derived from different -driven mice tumors treated with ATR inhibitors. The RUVBL proteins form a complex with ATPase activity that has broad cellular functions and we demonstrate that pharmacological inhibition of this protein complex results in a strong reduction of MYC(N) signaling, cell-cycle arrest, DNA damage, and apoptosis. We confirmed the association with and identified the genes as independent prognostic biomarkers in human primary neuroblastoma data. - Source: PubMed
Publication date: 2026/03/05
Siaw Joachim TettehClaeys ArneLai Wei-YunBorenäs MarcusHilgert ElienBekaert Sarah-LeeSanders EllenKaya IremVan Dorpe JoSpeleman FrankDurinck KaatHallberg BengtPalmer Ruth HVan den Eynden Jimmy - Postoperative delirium (POD) accelerates the transition from mild cognitive impairment (MCI) to Alzheimer's disease (AD) in elderly patients. Microglial metabolic reprogramming, a pivotal aspect of the immune-inflammatory response, modulates microglia-neuron interactions and postoperative cognitive function through microenvironmental alterations. Aberrant overexpression of RUVBL2 disrupts metabolic homeostasis, leading to stress granule (SG) aggregation and fibrosis. This study investigated the role of RUVBL2 in regulating metabolic reprogramming to mediate SG formation, with the aim of identifying novel prognostic targets for inhibiting glycolysis and mitigating POD-induced MCI progression. A POD model was established in aged MCI rats using 3% sevoflurane anesthesia for 3 h, combined with open reduction and internal fixation (ORIF). Multimodal magnetic resonance imaging (MRI) was employed to assess postoperative cognitive function. Glycolytic and oxidative phosphorylation (OXPHOS) activities in primary hippocampal microglia were quantified by extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). Lentiviral-mediated RUVBL2 expression modulation was performed to verify its role in microglial metabolic reprogramming. Postoperative hippocampal microglia underwent metabolic reprogramming from OXPHOS to glycolysis, with RUVBL2 expression correlating positively with POD progression. Elevated RUVBL2 expression drove metabolic reprogramming, while RUVBL2 knockdown inhibited this process, alleviated pro-inflammatory microglia-induced neuroinflammation and SG aggregation, and improved spontaneous neural activity and hippocampus-dependent cognitive deficits. In primary hippocampal microglia, RUVBL2 knockdown enhanced OXPHOS-related OCR and reduced glycolysis-associated ECAR, producing a synergistic neuroprotective effect. These findings reveal the critical role of RUVBL2 in regulating POD, highlight metabolic reprogramming as a novel therapeutic target, and suggest RUVBL2 as a promising intervention strategy for POD. - Source: PubMed
Zhang LinWang ZixuanYang ChenyiWang XinyiLiu XingZhang HaonanLiu HuanLiao HuihuiChen JunWang Haiyun - The pathophysiology of multiple sclerosis (MS) bears notable similarities to the dysregulated inflammatory response occurring during coronavirus disease 2019 (COVID-19) infection. B cells play a pivotal role among immune cells in the pathogenesis of both these diseases. Consequently, clarifying the molecular mechanism underlying B cell function in COVID-19 and MS is of great significance for formulating more efficient treatment strategies. A comprehensive analysis integrating single-cell RNA sequencing (scRNA-seq), genome-wide association study, and expression quantitative trait locus data from patients with COVID-19 and MS was performed. Gene set enrichment analysis revealed pathways and functional roles associated with the key genes, while pseudotime analysis tracked their expression patterns across different B cell developmental trajectories. The results of scRNA-seq analysis showed that, in comparison with the healthy control group, the proportion of B cells rose in patients with COVID-19 and those with MS. Through differential expression analysis and Mendelian randomization analysis, , , and were identified as risk factors for both COVID-19 and MS, whereas was characterized as a protective factor against these two conditions. The findings of the pseudotime analysis indicated that only had differential expression across different branches of B cells. 's role in promoting immune inflammation and inhibiting metabolism could potentially be linked to the onset and comorbidity of COVID-19 and MS. This emphasizes not only the possible interaction mechanisms between these two diseases but also their clinical significance. - Source: PubMed
Publication date: 2026/03/17
Chen ShupingRuan JunCheng SikaiZheng HuifangChang TianyuBao GuichunZhu ZijingLi XinglinZhao WeiZheng Kunwen