ArticleMolecular cell2015
A Protein Kinase C Phosphorylation Motif in GLUT1 Affects Glucose Transport and is Mutated in GLUT1 Deficiency Syndrome.
Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04137692 (Red Blood Cell Exchange Transfusion as a Novel Treatment for GLUT1 Deficiency Syndrome), which is not on this map. Cited by 72 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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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.
Red Blood Cell Exchange Transfusion as a Novel Treatment for GLUT1 Deficiency Syndrome
Who cites it
72 citing papers in PubMed, 153 citations in OpenAlex.
- Review
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- Metabolic reprogramming promotes apoptosis resistance in acute lymphoblastic leukemia through CASP3 lactylation.Molecular cancer · 2025Article
- Glut1 Deficiency Syndrome: Novel Pathomechanisms, Current Concepts, and Challenges.Journal of inherited metabolic disease · 2025Review
- Comprehensive Analysis of m6A-Related Programmed Cell Death Genes Unveils a Novel Prognostic Model for Lung Adenocarcinoma.Journal of cellular and molecular medicine · 2025Article
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- Identification of Potential Diagnostic Biomarkers of Carotid Atherosclerosis in Obese Populations.Journal of inflammation research · 2025Article
- Metabolic Targets in CRC: The Emerging Role of Cytochrome P450 Inhibitors.Current pharmaceutical design · 2025Review
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- A lactate-dependent shift of glycolysis mediates synaptic and cognitive processes in male mice.Nature communications · 2024Article
- Chrysophanol inhibits of colorectal cancer cell motility and energy metabolism by targeting the KITENIN/ErbB4 oncogenic complex.Cancer cell international · 2024Article
- GLUT1 overexpression enhances CAR T cell metabolic fitness and anti-tumor efficacy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Glycolytic enzymes in non-glycolytic web: functional analysis of the key players.Cell biochemistry and biophysics · 2024Review
- Endocytic vesicles act as vehicles for glucose uptake in response to growth factor stimulation.Nature communications · 2024Article
- Machine learning-mediated identification of ferroptosis-related genes in osteonecrosis of the femoral head.FEBS open bio · 2024Article
- Exploring shared therapeutic targets in diabetic cardiomyopathy and diabetic foot ulcers through bioinformatics analysis.Scientific reports · 2024Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Protein kinase C has been implicated in the phosphorylation of the erythrocyte/brain glucose transporter, GLUT1, without a clear understanding of the site(s) of phosphorylation and the possible effects on glucose transport. Through in vitro kinase assays, mass spectrometry, and phosphospecific antibodies, we identify serine 226 in GLUT1 as a PKC phosphorylation site. Phosphorylation of S226 is required for the rapid increase in glucose uptake and enhanced cell surface localization of GLUT1 induced by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Endogenous GLUT1 is phosphorylated on S226 in primary endothelial cells in response to TPA or VEGF. Several naturally occurring, pathogenic mutations that cause GLUT1 deficiency syndrome disrupt this PKC phosphomotif, impair the phosphorylation of S226 in vitro, and block TPA-mediated increases in glucose uptake. We demonstrate that the phosphorylation of GLUT1 on S226 regulates glucose transport and propose that this modification is important in the physiological regulation of glucose transport.
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