ArticleOncogene2008
Implication of human N-alpha-acetyltransferase 5 in cellular proliferation and carcinogenesis.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed.
- Yeast NatB Regulates Cell Death of Bax-Expressing Cells.Biomolecules · 2025Article
- Illuminating the impact of N-terminal acetylation: from protein to physiology.Nature communications · 2025Review
- NatB Protects Procaspase-8 from UBR4-Mediated Degradation and Is Required for Full Induction of the Extrinsic Apoptosis Pathway.Molecular and cellular biology · 2024Article
- Impact of Protein NLife (Basel, Switzerland) · 2023Review
- Semi-Synthetic CoA-α-Synuclein Constructs Trap N-Terminal Acetyltransferase NatB for Binding Mechanism Studies.Journal of the American Chemical Society · 2023Article
- How important is the N-terminal acetylation of alpha-synuclein for its function and aggregation into amyloids?Frontiers in neuroscience · 2022Review
- Structural basis of Naa20 activity towards a canonical NatB substrate.Communications biology · 2021Article
- Identification of NAA40 as a Potential Prognostic Marker for Aggressive Liver Cancer Subtypes.Frontiers in oncology · 2021Article
- Protein acetylation and deacetylation: An important regulatory modification in gene transcription (Review).Experimental and therapeutic medicine · 2020Review
- Article
- NatB-Mediated N-Terminal Acetylation Affects Growth and Biotic Stress Responses.Plant physiology · 2020Article
- Structure and Mechanism of Acetylation by the N-Terminal Dual Enzyme NatA/Naa50 Complex.Structure (London, England : 1993) · 2019Article
- Spotlight on protein N-terminal acetylation.Experimental & molecular medicine · 2018Review
- NatB-mediated protein N-α-terminal acetylation is a potential therapeutic target in hepatocellular carcinoma.Oncotarget · 2017Article
- Naa50/San-dependent N-terminal acetylation of Scc1 is potentially important for sister chromatid cohesion.Scientific reports · 2016Article
- High expression of Naa10p associates with lymph node metastasis and predicts favorable prognosis of oral squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Depletion of histone N-terminal-acetyltransferase Naa40 induces p53-independent apoptosis in colorectal cancer cells via the mitochondrial pathway.Apoptosis : an international journal on programmed cell death · 2016Article
- Absence of N-terminal acetyltransferase diversification during evolution of eukaryotic organisms.Scientific reports · 2016Article
- Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.Molecular cancer · 2015Article
- New roles for old modifications: emerging roles of N-terminal post-translational modifications in development and disease.Protein science : a publication of the Protein Society · 2014Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The N-alpha-acetyltransferase NatB, composed in Saccharomyces cerevisiae by the Nat3p and Mdm20p subunits, is an important factor for yeast growth and resistance to several stress agents. However, the expression and functional role of the mammalian counterpart has not yet been analysed. Here, we report the identification of Nat3p human homologue (hNAT5/hNAT3) and the characterization of its biological function. We found that hNAT5/hNAT3 silencing in HeLa cells results in inhibition of cell proliferation and increased sensitivity to the pro-apoptotic agent MG132. Moreover, inhibition of hNAT5/hNAT3 expression induces p53 activation and upregulation of the antiproliferative protein p21(WAF1/CIP1). The changes of the cellular transcriptome after hNAT5/hNAT3 knockdown confirmed the involvement of this protein in cell growth and survival processes. Among the genes differentially expressed, we observed upregulation of several p53-dependent antiproliferative and pro-apoptotic genes. In the c-myc transgenic mice, which is a model of inducible hepatocarcinoma, we found that hNAT5/hNAT3 was upregulated when the tumour was induced. In accordance with this observation, we noticed increased hNAT5/hNAT3 protein level in neoplastic versus non-neoplastic tissue in a high proportion of patients with hepatocellular carcinoma. Consequently, our results suggest that hNAT5/hNAT3 is required for cellular proliferation and can be implicated in tumour growth.
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Registered trials
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