ArticlePloS one2013
RABL6A, a novel RAB-like protein, controls centrosome amplification and chromosome instability in primary fibroblasts.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Revealing RELL1 signaling relying on the phosphoregulatory network analysis.Frontiers in bioinformatics · 2026Article
- CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- The oncogenic potential of Rab-like protein 1A (RBEL1A) GTPase: The first review of RBEL1A research with future research directions and challenges.Journal of Cancer · 2023Review
- The Role of CDK Pathway Dysregulation and Its Therapeutic Potential in Soft Tissue Sarcoma.Cancers · 2022Review
- Fine-tuning cell organelle dynamics during mitosis by small GTPases.Frontiers of medicine · 2022Review
- Endocytic membrane trafficking in the control of centrosome function.Current opinion in cell biology · 2020Review
- High expression of RABL6 promotes cell proliferation and predicts poor prognosis in esophageal squamous cell carcinoma.BMC cancer · 2020Article
- RABL6A Is an Essential Driver of MPNSTs that Negatively Regulates the RB1 Pathway and Sensitizes Tumor Cells to CDK4/6 Inhibitors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- A novel prognostic marker of non-small cell lung cancer: chromosome 9 open reading frame 86 (Journal of thoracic disease · 2016Article
- TRIM28 Is an E3 Ligase for ARF-Mediated NPM1/B23 SUMOylation That Represses Centrosome Amplification.Molecular and cellular biology · 2015Article
- RABL6A promotes G1-S phase progression and pancreatic neuroendocrine tumor cell proliferation in an Rb1-dependent manner.Cancer research · 2014Article
- Oncogenic RABL6A promotes NF1-associated MPNST progression in vivo.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
RABL6A (RAB-like 6 isoform A) is a novel protein that was originally identified based on its association with the Alternative Reading Frame (ARF) tumor suppressor. ARF acts through multiple p53-dependent and p53-independent pathways to prevent cancer. How RABL6A functions, to what extent it depends on ARF and p53 activity, and its importance in normal cell biology are entirely unknown. We examined the biological consequences of RABL6A silencing in primary mouse embryo fibroblasts (MEFs) that express or lack ARF, p53 or both proteins. We found that RABL6A depletion caused centrosome amplification, aneuploidy and multinucleation in MEFs regardless of ARF and p53 status. The centrosome amplification in RABL6A depleted p53-/- MEFs resulted from centrosome reduplication via Cdk2-mediated hyperphosphorylation of nucleophosmin (NPM) at threonine-199. Thus, RABL6A prevents centrosome amplification through an ARF/p53-independent mechanism that restricts NPM-T199 phosphorylation. These findings demonstrate an essential role for RABL6A in centrosome regulation and maintenance of chromosome stability in non-transformed cells, key processes that ensure genomic integrity and prevent tumorigenesis.
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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.