ArticleLeukemia2013
The AAA+ ATPase RUVBL2 is a critical mediator of MLL-AF9 oncogenesis.
Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- RUVBL1/2 Blockade Targets YTHDF1 Activity to Suppress m6A-Dependent Oncogenic Translation and Colorectal Tumorigenesis.Cancer research · 2024Article
- Article
- Genetic and chemical targeting of the ATPase complex TIP48 and 49 impairs acute myeloid leukemia.Leukemia · 2023Article
- A Systematic Analysis Reveals the Prognostic and Immunological Role of Reptin/RUVBL2 in Human Tumors.Frontiers in genetics · 2022Article
- Ruvbl2 Suppresses Cardiomyocyte Proliferation During Zebrafish Heart Development and Regeneration.Frontiers in cell and developmental biology · 2022Article
- CoRe: a robustly benchmarked R package for identifying core-fitness genes in genome-wide pooled CRISPR-Cas9 screens.BMC genomics · 2021Article
- The ATPase Pontin is a key cell cycle regulator by amplifying E2F1 transcription response in glioma.Cell death & disease · 2021Article
- EVI1 phosphorylation at S436 regulates interactions with CtBP1 and DNMT3A and promotes self-renewal.Cell death & disease · 2020Article
- Sorafenib as an Inhibitor of RUVBL2.Biomolecules · 2020Article
- LOC101060264 Silencing Suppresses Invasion and Metastasis of Human Colon Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- RUVBL1/RUVBL2 ATPase Activity Drives PAQosome Maturation, DNA Replication and Radioresistance in Lung Cancer.Cell chemical biology · 2020Article
- The AAA+ATPase RUVBL2 is essential for the oncogenic function of c-MYB in acute myeloid leukemia.Leukemia · 2019Article
- Turning Stem Cells Bad: Generation of Clinically Relevant Models of Human Acute Myeloid Leukemia through Gene Delivery- or Genome Editing-Based Approaches.Molecules (Basel, Switzerland) · 2018Review
- Article
- The Role of Pontin and Reptin in Cellular Physiology and Cancer Etiology.Frontiers in molecular biosciences · 2017Review
- Proteomic characterization of peroxisome proliferator-activated receptor-γ (PPARγ) overexpressing or silenced colorectal cancer cells unveils a novel protein network associated with an aggressive phenotype.Molecular oncology · 2016Article
- Feature genes predicting the FLT3/ITD mutation in acute myeloid leukemia.Molecular medicine reports · 2016Article
- Proton irradiation impacts age-driven modulations of cancer progression influenced by immune system transcriptome modifications from splenic tissue.Journal of radiation research · 2015Article
- Article
- The AAA+ proteins Pontin and Reptin enter adult age: from understanding their basic biology to the identification of selective inhibitors.Frontiers in molecular biosciences · 2015Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
The most frequent chromosomal translocations in pediatric acute myeloid leukemia affect the 11q23 locus and give rise to mixed lineage leukemia (MLL) fusion genes, MLL-AF9 being the most prevalent. The MLL-AF9 fusion gene has been shown to induce leukemia in both mouse and human models. In this study, we demonstrate that leukemogenic activity of MLL-AF9 requires RUVBL2 (RuvB-like 2), an AAA+ ATPase family member that functions in a wide range of cellular processes, including chromatin remodeling and transcriptional regulation. Expression of RUVBL2 was dependent on MLL-AF9, as it increased upon immortalization of human cord blood-derived hematopoietic progenitor cells with the fusion gene and decreased following loss of fusion gene expression in conditionally immortalized mouse cells. Short hairpin RNA-mediated silencing experiments demonstrated that both the immortalized human cells and the MLL-AF9-expressing human leukemia cell line THP-1 required RUVBL2 expression for proliferation and survival. Furthermore, inhibition of RUVBL2 expression in THP-1 cells led to reduced telomerase activity and clonogenic potential. These data were confirmed with a dominant-negative Walker B-mutated RUVBL2 construct. Taken together, these data suggest the possibility of targeting RUVBL2 as a potential therapeutic strategy for MLL-AF9-associated leukemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.