ArticlePloS one2014
Nuclear translocation of hARD1 contributes to proper cell cycle progression.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- NAA10 (N-Alpha-Acetyltransferase 10): A Multifunctional Regulator in Development, Disease, and Cancer.Cells · 2025Review
- NAA10 as a New Prognostic Marker for Cancer Progression.International journal of molecular sciences · 2020Review
- NAA50 Is an Enzymatically ActivePlant physiology · 2020Article
- Characterization of Lysine Acetyltransferase Activity of Recombinant Human ARD1/NAA10.Molecules (Basel, Switzerland) · 2020Article
- Spotlight on protein N-terminal acetylation.Experimental & molecular medicine · 2018Review
- ARD1/NAA10 in hepatocellular carcinoma: pathways and clinical implications.Experimental & molecular medicine · 2018Review
- The Role of N-α-acetyltransferase 10 Protein in DNA Methylation and Genomic Imprinting.Molecular cell · 2017Article
- SAMHD1 acetylation enhances its deoxynucleotide triphosphohydrolase activity and promotes cancer cell proliferation.Oncotarget · 2017Article
- The torments of the cohesin ring.Nucleus (Austin, Tex.) · 2017Review
- Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arrest defective 1 (ARD1) is an acetyltransferase that is highly conserved across organisms, from yeasts to humans. The high homology and widespread expression of ARD1 across multiple species and tissues signify that it serves a fundamental role in cells. Human ARD1 (hARD1) has been suggested to be involved in diverse biological processes, and its role in cell proliferation and cancer development has been recently drawing attention. However, the subcellular localization of ARD1 and its relevance to cellular function remain largely unknown. Here, we have demonstrated that hARD1 is imported to the nuclei of proliferating cells, especially during S phase. Nuclear localization signal (NLS)-deleted hARD1 (hARD1ΔN), which can no longer access the nucleus, resulted in cell morphology changes and cellular growth impairment. Notably, hARD1ΔN-expressing cells showed alterations in the cell cycle and the expression levels of cell cycle regulators compared to hARD1 wild-type cells. Furthermore, these effects were rescued when the nuclear import of hARD1 was restored by exogenous NLS. Our results show that hARD1 nuclear translocation mediated by NLS is required for cell cycle progression, thereby contributing to proper cell 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.