ArticleFEBS open bio2016
FGT-1-mediated glucose uptake is defective in insulin/IGF-like signaling mutants in Caenorhabditis elegans.
Article in FEBS open bio, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Yolk-deprivedLife science alliance · 2023Article
- Anti-Hyperglycemic Effects of Oils and Extracts Derived from Sea Buckthorn - A Comprehensive Analysis Utilizing In Vitro and In Vivo Models.Molecular nutrition & food research · 2022Article
- Tandem Mass Tagging (TMT) Reveals Tissue-Specific Proteome of L4 Larvae ofInternational journal of molecular sciences · 2022Article
- Review
- Elevated Trehalose Levels inMetabolites · 2021Article
- Caenorhabditis elegans respond to high-glucose diets through a network of stress-responsive transcription factors.PloS one · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Insulin signaling plays a central role in the regulation of facilitative glucose transporters (GLUTs) in humans. To establish Caenorhabditis elegans (C. elegans) as a model to study the mechanism underlying insulin regulation of GLUT, we identified that FGT-1 is most likely the only functional GLUT homolog in C. elegans and is ubiquitously expressed. The FGT-1-mediated glucose uptake was almost completely defective in insulin/IGF-like signaling (IIS) mutants daf-2 and age-1, and this defect mainly resulted from the down-regulated FGT-1 protein expression. However, glycosylation may also be involved because OGA-1, an O-GlcNAcase, was essential for the function of FGT-1. Thus, our study showed that C. elegans can be a new powerful model system to study insulin regulation of GLUT.
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