ReviewOncogene2013
Protein N-terminal acetyltransferases in cancer.
Review in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 168 citations in OpenAlex.
- Mechanisms of Congenital Heart Disease Caused by NAA15 Haploinsufficiency.Circulation research · 2021Trial
- Inhibition of N-Terminal Acetyltransferase C Mitigates Endoplasmic Reticulum Stress-Mediated Muscle Atrophy in Cancer Cachexia.Journal of cachexia, sarcopenia and muscle · 2026Article
- NAA60 facilitates LRRC8A- and LRRC8D-mediated platinum drug uptake.Communications biology · 2025Article
- ATE1 promotes breast cancer progression via arginylation-dependent regulation of MAPK-MYC signaling.Cell communication and signaling : CCS · 2025Article
- NAA10 (N-Alpha-Acetyltransferase 10): A Multifunctional Regulator in Development, Disease, and Cancer.Cells · 2025Review
- Multi-protein assemblies orchestrate co-translational enzymatic processing on the human ribosome.Nature communications · 2024Article
- NAA60 (HAT4): the newly discovered bi-functional Golgi member of the acetyltransferase family.Clinical epigenetics · 2022Review
- Naa10p promotes cell invasiveness of esophageal cancer by coordinating the c-Myc and PAI1 regulatory axis.Cell death & disease · 2022Article
- Extended N-Terminal Acetyltransferase Naa50 in Filamentous Fungi Adds to Naa50 Diversity.International journal of molecular sciences · 2022Article
- Biochemical analysis of novel NAA10 variants suggests distinct pathogenic mechanisms involving impaired protein N-terminal acetylation.Human genetics · 2022Article
- Evidence that the transcriptional repressor ICER is regulated via the N-end rule for ubiquitination.Experimental cell research · 2022Article
- N-α-Acetyltransferase 10 inhibits invasion and metastasis of oral squamous cell carcinoma via regulating Pirh2-p53 signalling pathway.Journal of cellular and molecular medicine · 2022Article
- Adaptive Response ofJournal of fungi (Basel, Switzerland) · 2022Article
- Cotranslational N-degron masking by acetylation promotes proteome stability in plants.Nature communications · 2022Article
- Pan-cancer analysis reveals NAA50 as a cancer prognosis and immune infiltration-related biomarker.Frontiers in genetics · 2022Article
- Lysine Acetyltransferases and Their Role in AR Signaling and Prostate Cancer.Frontiers in endocrinology · 2022Review
- Mini-review: Recent advances in post-translational modification site prediction based on deep learning.Computational and structural biotechnology journal · 2022Review
- caAtlas: An immunopeptidome atlas of human cancer.iScience · 2021Article
- Molecular mechanism of N-terminal acetylation by the ternary NatC complex.Structure (London, England : 1993) · 2021Article
- Naa10p and IKKα interaction regulates EMT in oral squamous cell carcinoma via TGF-β1/Smad pathway.Journal of cellular and molecular medicine · 2021Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human N-terminal acetyltransferases (NATs) catalyze the transfer of acetyl moieties to the N-termini of 80-90% of all human proteins. Six NAT types are present in humans, NatA-NatF, each is composed of specific subunits and each acetylates a set of substrates defined by the N-terminal amino-acid sequence. NATs have been suggested to act as oncoproteins as well as tumor suppressors in human cancers, and NAT expression may be both elevated and decreased in cancer versus non-cancer tissues. Manipulation of NATs in cancer cells induced cell-cycle arrest, apoptosis or autophagy, implying that these enzymes target a variety of pathways. Of particular interest is hNaa10p (human ARD1), the catalytic subunit of the NatA complex, which was coupled to a number of signaling molecules including hypoxia inducible factor-1α, β-catenin/cyclin D1, TSC2/mammalian target of rapamycin, myosin light chain kinase , DNA methyltransferase1/E-cadherin and p21-activated kinase-interacting exchange factors (PIX)/Cdc42/Rac1. The variety of mechanistic links where hNaa10p acts as a NAT, a lysine acetyltransferase or displaying a non-catalytic role, provide insights to how hNaa10p may act as both a tumor suppressor and oncoprotein.
Indexed as
Identifiers
What OpenQuestion holds
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.