ArticlePloS one2015
Chromosome Missegregation Associated with RUVBL1 Deficiency.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- The multitalented TIP60 chromatin remodeling complex: wearing many hats in epigenetic regulation, cell division and diseases.Epigenetics & chromatin · 2025Review
- Expression of foetal gene Pontin is essential in protecting heart against pathological remodelling and cardiomyopathy.Nature communications · 2025Article
- Molecular profile of bladder cancer progression to clinically aggressive subtypes.Nature reviews. Urology · 2024Review
- Structural differences between the closely related RNA helicases, UAP56 and URH49, fashion distinct functional apo-complexes.Nature communications · 2024Article
- Unconventional roles of chromatin remodelers and long non-coding RNAs in cell division.Cellular and molecular life sciences : CMLS · 2023Review
- Combined CRISPRi and proteomics screening reveal a cohesin-CTCF-bound allele contributing to increased expression of RUVBL1 and prostate cancer progression.American journal of human genetics · 2023Article
- Downregulation of AHNAK2 inhibits cell cycle of lung adenocarcinoma cells by interacting with RUVBL1.Thoracic cancer · 2023Article
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- RUVBL1-modulated chromatin remodeling alters the transcriptional activity of oncogenic CTNNB1 in uveal melanoma.Cell death discovery · 2023Article
- Drug repositioning prediction for psoriasis using the adverse event reporting database.Frontiers in medicine · 2023Article
- Evolutionary conserved relocation of chromatin remodeling complexes to the mitotic apparatus.BMC biology · 2022Article
- Clinicopathological Review of Micropapillary Urothelial Carcinoma.Current oncology reports · 2022Review
- A Systematic Analysis Reveals the Prognostic and Immunological Role of Reptin/RUVBL2 in Human Tumors.Frontiers in genetics · 2022Article
- The ATPase SRCAP is associated with the mitotic apparatus, uncovering novel molecular aspects of Floating-Harbor syndrome.BMC biology · 2021Article
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- Article
- RUVBL1/RUVBL2 ATPase Activity Drives PAQosome Maturation, DNA Replication and Radioresistance in Lung Cancer.Cell chemical biology · 2020Article
- The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer.Cancers · 2019Review
- The R2TP complex regulates paramyxovirus RNA synthesis.PLoS pathogens · 2019Article
- Identification of RUVBL1 and RUVBL2 as Novel Cellular Interactors of the Ebola Virus Nucleoprotein.Viruses · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RUVBL1 (RuvB-like1) and RUVBL2 (RuvB-like 2) are integral components of multisubunit protein complexes involved in processes ranging from cellular metabolism, transcription and chromatin remodeling to DNA repair. Here, we show that although RUVBL1 and RUVBL2 are known to form heterodimeric complexes in which they stabilize each other, the subunits separate during cytokinesis. In anaphase-to-telophase transition, RUVBL1 localizes to structures of the mitotic spindle apparatus, where it partially co-localizes with polo-like kinase 1 (PLK1). The ability of PLK1 to phosphorylate RUVBL1-but not RUVBL2-in vitro and their physical association in vivo suggest that this kinase differentially regulates the function of the RuvB-like proteins during mitosis. We further show that siRNA-mediated knock-down of RuvB-like proteins causes severe defects in chromosome alignment and segregation. In addition, we show that the ATPase activity of RUVBL1 is indispensable for cell proliferation. Our data thus demonstrate that RUVBL1 is essential for efficient mitosis and proliferation.
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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.