ArticleScientific reports2014
Phenylalanine sensitive K562-D cells for the analysis of the biochemical impact of excess amino acid.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- A Comparative Analysis of Oxidative Stress and Inflammatory Biomarkers in Different Stages of Endometriosis.Journal of reproduction & infertility · 2025Article
- Methionine-triggered growth arrest reveals activation of Gcn2 by methionine transporter endocytosis.bioRxiv : the preprint server for biology · 2025Article
- Growth Inhibition by Amino Acids inMicroorganisms · 2020Article
- Ectopic overexpression of Kir6.1 in the mouse heart impacts on the life expectancy.Scientific reports · 2018Article
- Phenylalanine regulates initiation of digestive enzyme mRNA translation in pancreatic acinar cells and tissue segments in dairy calves.Bioscience reports · 2018Article
- Post-Translational Incorporation of L-Phenylalanine into the C-Terminus of α-Tubulin as a Possible Cause of Neuronal Dysfunction.Scientific reports · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Although it is recognized that the abnormal accumulation of amino acid is a cause of the symptoms in metabolic disease such as phenylketonuria (PKU), the relationship between disease severity and serum amino acid levels is not well understood due to the lack of experimental model. Here, we present a novel in vitro cellular model using K562-D cells that proliferate slowly in the presence of excessive amount of phenylalanine within the clinically observed range, but not phenylpyruvate. The increased expression of the L-type amino acid transporter (LAT2) and its adapter protein 4F2 heavy chain appeared to be responsible for the higher sensitivity to phenylalanine in K562-D cells. Supplementation with valine over phenylalanine effectively restored cell proliferation, although other amino acids did not improve K562-D cell proliferation over phenylalanine. Biochemical analysis revealed mammalian target of rapamycin complex (mTORC) as a terminal target of phenylalanine in K562-D cell proliferation, and supplementation of valine restored mTORC1 activity. Our results show that K562-D cell can be a potent tool for the investigation of PKU at the molecular level and to explore new therapeutic approaches to the disease.
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