RVB1 Antibody
- Known as:
- RVB1 Antibody
- Catalog number:
- XW-7681
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- RVB1 Antibody
Related genes to: RVB1 Antibody
- Gene:
- RUVBL1 NIH gene
- Name:
- RuvB like AAA ATPase 1
- Previous symbol:
- -
- Synonyms:
- TIP49, NMP238, RVB1, TIP49a, Pontin52, ECP54, TIH1, Rvb1, INO80H
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-19
- Date modifiied:
- 2016-10-05
Related products to: RVB1 Antibody
Related articles to: RVB1 Antibody
- PIWI proteins, a subfamily of the PAZ-PIWI domain (PPD) protein family, are traditionally regarded as germline factors that partner with PIWI-interacting RNAs (piRNAs) to silence transposons and regulate gene expression. However, growing evidence implicates PIWI proteins as oncogenic drivers in diverse somatic cancers, often acting through piRNA-independent mechanisms that remain incompletely understood. Here, we integrate transcriptomic, translatomic, and proteomic profiling of wild-type versus PIWIL1-knockout gastric cancer cells to uncover a non-canonical, translational role for PIWIL1, one of the four human PIWI proteins. We find that PIWIL1 selectively enhances the translation of 5'-terminal oligopyrimidine (TOP) mRNAs by activating mTOR complex 1 (mTORC1). Mechanistically, PIWIL1 interacts with the R2TP chaperone complex (RUVBL1-RUVBL2-RPAP3-PIH1D1) and promotes its association with TELO2, facilitating mTOR-RAPTOR assembly and mTORC1 activation. Functionally, PIWIL1 deficiency sensitizes gastric cancer cells to mTOR inhibition, and in clinical samples, PIWIL1 expression positively correlates with mTORC1 pathway activity. Together, these findings define a novel piRNA-independent mechanism through which PIWIL1 contributes to tumor progression, extend PIWI-mediated translational control from the germline to human cancers, and establish PIWIL1 as a potential therapeutic target for gastric cancer in synergy with mTOR inhibition. - Source: PubMed
Publication date: 2026/04/22
Fan TianquZhao JiangshaLi LingCui MeihuaZhang JiaweiChi TianShi Shuo - 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 - RuvB-like protein 1 (RUVBL1) has been reported to be associated with tumor progression in various cancers. However, its role in colon adenocarcinoma (COAD) remains poorly understood. - Source: PubMed
Publication date: 2026/04/16
Wu DabinLiu HuilingXu XuesongLiu Hang - The AAA+ ATPase RuvBL1 takes part in several biological processes, including chromatin remodelling and DNA repair, ribosome biogenesis, mTOR signalling, and oncogenic transformation. RUVBL1 overexpression correlates with poor survival in hepatocellular carcinoma patients. We previously found that RuvBL1 is a key regulator of liver glucose metabolism in mice. Here, we aimed at disentangling the metabolic function of RuvBL1 in HCC cells. - Source: PubMed
Publication date: 2026/04/17
Mello TommasoSimeone IreneGuida AlicePapini DimitriBegnozzi FrancescaSanti AliceGuasti DanieleNardini PatriziaPolvani SimoneLulli MatteoBereshchenko OxanaCeni ElisabettaCurto ArmandoPinton PaoloBonora MassimoGalli Andrea - MAPK signaling is key for osteogenic differentiation of periodontal ligament stem cells (PDLSCs), a process important in treating periodontal injury. RuvB‑like AAA ATPase‑1 (RUVBL1) binds C‑Raf proto‑oncogene serine/threonine‑protein kinase (CRAF) to activate the MAPK signaling pathway, but the specific roles and mechanisms of RUVBL1 and CRAF in PDLSCs remain unclear. In the present study, PDLSCs were subjected to lentiviral transfection for RUVBL1 and CRAF expression manipulation. Flow cytometry was performed to characterize mesenchymal SC (MSC) features. A Cell Counting Kit‑8 assay was used to assess PDLSC proliferative viability. Lipogenic differentiation potential was evaluated using Oil Red O staining following lipogenic induction. Alkaline phosphatase and alizarin red staining were utilized to assess osteogenic differentiation potential and mineralization, respectively, following osteogenic induction. Reverse transcription‑quantitative PCR and western blotting were conducted to determine the effects of RUVBL1 and CRAF on the MAPK signaling pathway in PCLSCs. PDLSCs were determined to be SCs exhibiting self‑renewal and MSC characteristics, including lipogenic and osteogenic differentiation potential. RUVBL1 overexpression enhanced PDLSC osteogenic differentiation while inhibiting proliferative activity and lipogenic differentiation. Conversely, CRAF overexpression promoted PDLSC proliferative activity, as well as osteogenic and lipogenic differentiation. Knockdown of RUVBL1 reduced osteogenic differentiation while enhancing proliferative activity and lipogenic differentiation, whereas knockdown of CRAF suppressed proliferative activity, osteogenic differentiation and lipogenic differentiation. RUVBL1 did not regulate CRAF in PDLSCs. However, overexpression of RUVBL1 or CRAF promoted MEK and ERK phosphorylation, activating the MEK/ERK signaling pathway. Overall, RUVBL1 and CRAF activated the MEK/ERK signaling pathway to promote osteogenic differentiation in PDLSCs, although RUVBL1 did not regulate CRAF. - Source: PubMed
Publication date: 2026/04/17
Zhang Xin-YuHao PeiqiQi Ming-YueGuo Hui