ArticleFEBS letters2022
Arginyl-tRNA-protein transferase 1 (ATE1) promotes melanoma cell growth and migration.
Article in FEBS letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed, 6 citations in OpenAlex.
- The C-terminal domain of yeast Arginyltransferase1 is essential for its catalytic activity.FEBS open bio · 2026Article
- Proteomic Analysis Identifies ATE1-Dependent Arginylation Dysregulation across Meningioma Grades.Journal of proteome research · 2026Article
- Trypsin exhibits exopeptidase-like activity toward N-terminal arginine that biases proteomic analyses.bioRxiv : the preprint server for biology · 2026Article
- ATE1 promotes breast cancer progression via arginylation-dependent regulation of MAPK-MYC signaling.Cell communication and signaling : CCS · 2025Article
- Structure and Mechanism of Aminoacyl-tRNA-Protein L/F- and R-transferases.Journal of molecular biology · 2025Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
Abstract
Arginyl-tRNA-protein transferase 1 (ATE1) catalyses N-terminal protein arginylation, a post-translational modification implicated in cell migration, invasion and the cellular stress response. Herein, we report that ATE1 is overexpressed in NRAS-mutant melanomas, while it is downregulated in BRAF-mutant melanomas. ATE1 expression was higher in metastatic tumours, compared with primary tumours. Consistent with these findings, ATE1 depletion reduced melanoma cell viability, migration and colony formation. Reduced ATE1 expression also affected cell responses to mTOR and MEK inhibitors and to serum deprivation. Among putative ATE1 substrates is the tumour suppressor AXIN1, pointing to the possibility that ATE1 may fine-tune AXIN1 function in melanoma. Our findings highlight an unexpected role for ATE1 in melanoma cell aggressiveness and suggest that ATE1 constitutes a potential new therapeutic target.
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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.