ArticleThe Journal of general physiology2007
Structural basis of GLUT1 inhibition by cytoplasmic ATP.
Article in The Journal of general physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 94 citations in OpenAlex.
- Red blood cells serve as a primary glucose sink to improve glucose tolerance at altitude.Cell metabolism · 2026Article
- Glut1 Deficiency Syndrome: Novel Pathomechanisms, Current Concepts, and Challenges.Journal of inherited metabolic disease · 2025Review
- Chitinase-1 inhibition attenuates metabolic dysregulation and restores homeostasis in MASH animal models.Frontiers in immunology · 2025Article
- Differentially expressed genes associated with high metabolic tumor volume served as diagnostic markers and potential therapeutic targets for pancreatic cancer.Journal of translational medicine · 2024Article
- The novel family of WarbicinFrontiers in oncology · 2024Article
- Pericytes and the Control of Blood Flow in Brain and Heart.Annual review of physiology · 2023Review
- Regulatory Mechanism on Anti-Glycolytic and Anti-Metastatic Activities Induced byPharmaceuticals (Basel, Switzerland) · 2023Article
- The transition between acute and chronic infections in light of energy control: a mathematical model of energy flow in response to infection.Journal of the Royal Society, Interface · 2022Article
- Paracrine HB-EGF signaling reduce enhanced contractile and energetic state of activated decidual fibroblasts by rebalancing SRF-MRTF-TCF transcriptional axis.Frontiers in cell and developmental biology · 2022Article
- LncRNA HOTAIR regulates glucose transporter Glut1 expression and glucose uptake in macrophages during inflammation.Scientific reports · 2021Article
- Glucose transporters in pancreatic islets.Pflugers Archiv : European journal of physiology · 2020Review
- Kinetic Basis of Cis- and Trans-Allostery in GLUT1-Mediated Sugar Transport.The Journal of membrane biology · 2018Article
- Reconciling contradictory findings: Glucose transporter 1 (GLUT1) functions as an oligomer of allosteric, alternating access transporters.The Journal of biological chemistry · 2017Article
- Affinity and path of binding xylopyranose unto E. coli xylose permease.Biochemical and biophysical research communications · 2017Article
- Caffeine inhibition of GLUT1 is dependent on the activation state of the transporter.Biochimie · 2017Article
- GLUT1-mediated glucose uptake plays a crucial role during Plasmodium hepatic infection.Cellular microbiology · 2017Article
- SLC2A8 (GLUT8) is a mammalian trehalose transporter required for trehalose-induced autophagy.Scientific reports · 2016Article
- How does the chemical potential of the substrate drive a uniporter?Protein science : a publication of the Protein Society · 2016Article
- Understanding transport by the major facilitator superfamily (MFS): structures pave the way.Nature reviews. Molecular cell biology · 2016Review
- Mitoenergetic Dysfunction Triggers a Rapid Compensatory Increase in Steady-State Glucose Flux.Biophysical journal · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cytoplasmic ATP inhibits human erythrocyte glucose transport protein (GLUT1)-mediated glucose transport in human red blood cells by reducing net glucose transport but not exchange glucose transport (Cloherty, E.K., D.L. Diamond, K.S. Heard, and A. Carruthers. 1996. Biochemistry. 35:13231-13239). We investigated the mechanism of ATP regulation of GLUT1 by identifying GLUT1 domains that undergo significant conformational change upon GLUT1-ATP interaction. ATP (but not GTP) protects GLUT1 against tryptic digestion. Immunoblot analysis indicates that ATP protection extends across multiple GLUT1 domains. Peptide-directed antibody binding to full-length GLUT1 is reduced by ATP at two specific locations: exofacial loop 7-8 and the cytoplasmic C terminus. C-terminal antibody binding to wild-type GLUT1 expressed in HEK cells is inhibited by ATP but binding of the same antibody to a GLUT1-GLUT4 chimera in which loop 6-7 of GLUT1 is substituted with loop 6-7 of GLUT4 is unaffected. ATP reduces GLUT1 lysine covalent modification by sulfo-NHS-LC-biotin by 40%. AMP is without effect on lysine accessibility but antagonizes ATP inhibition of lysine modification. Tandem electrospray ionization mass spectrometry analysis indicates that ATP reduces covalent modification of lysine residues 245, 255, 256, and 477, whereas labeling at lysine residues 225, 229, and 230 is unchanged. Exogenous, intracellular GLUT1 C-terminal peptide mimics ATP modulation of transport whereas C-terminal peptide-directed IgGs inhibit ATP modulation of glucose transport. These findings suggest that transport regulation involves ATP-dependent conformational changes in (or interactions between) the GLUT1 C terminus and the C-terminal half of GLUT1 cytoplasmic loop 6-7.
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.