ArticleThe EMBO journal2012
Hypoxia regulates glutamate receptor trafficking through an HIF-independent mechanism.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- Role of ubiquitin‑proteasome system in preeclampsia (Review).Molecular medicine reports · 2026Review
- The Physiological and Pathological Mechanisms of LIN2, LIN7, LIN10 and Their Tripartite Complex.Journal of cellular and molecular medicine · 2025Review
- Transcriptome analyses describe the consequences of persistent HIF-1 over-activation in Caenorhabditis elegans.PloS one · 2024Article
- The Brain at High Altitude: From Molecular Signaling to Cognitive Performance.International journal of molecular sciences · 2023Review
- Article
- Surface acoustic wave microfluidics for repetitive and reversible temporary immobilization ofLab on a chip · 2022Article
- The hypoxia response pathway promotes PEP carboxykinase and gluconeogenesis in C. elegans.Nature communications · 2022Article
- The signaling pathway of levamisole-sensitive-acetylcholine receptors involved in short-term forgetting of Caenorhabditis elegans.Molecular genetics and genomics : MGG · 2022Article
- Hypoxic stress disrupts HGF/Met signaling in human trophoblasts: implications for the pathogenesis of preeclampsia.Journal of biomedical science · 2022Article
- VER/VEGF receptors regulate AMPA receptor surface levels and glutamatergic behavior.PLoS genetics · 2021Article
- Crosstalk in oxygen homeostasis networks: SKN-1/NRF inhibits the HIF-1 hypoxia-inducible factor in Caenorhabditis elegans.PloS one · 2021Article
- Human Red Blood Cells Modulate Cytokine Expression in Monocytes/Macrophages Under Anoxic Conditions.Frontiers in physiology · 2021Article
- Hypoxic response regulators RHY-1 and EGL-9/PHD promote longevity through a VHL-1-independent transcriptional response.GeroScience · 2020Article
- An Experimentally Defined Hypoxia Gene Signature in Glioblastoma and Its Modulation by Metformin.Biology · 2020Article
- Endocytosis in the adaptation to cellular stress.Cell stress · 2020Review
- The hypoxia-response pathway modulates RAS/MAPK-mediated cell fate decisions inLife science alliance · 2019Article
- Cell Biology of the Mitochondrion.Genetics · 2017Review
- The Effects of Hypoxia and Inflammation on Synaptic Signaling in the CNS.Brain sciences · 2016Review
- Article
- Phenotypic switch of CD8(+) T cells reactivated under hypoxia toward IL-10 secreting, poorly proliferative effector cells.European journal of immunology · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Oxygen influences behaviour in many organisms, with low levels (hypoxia) having devastating consequences for neuron survival. How neurons respond physiologically to counter the effects of hypoxia is not fully understood. Here, we show that hypoxia regulates the trafficking of the glutamate receptor GLR-1 in C. elegans neurons. Either hypoxia or mutations in egl-9, a prolyl hydroxylase cellular oxygen sensor, result in the internalization of GLR-1, the reduction of glutamate-activated currents, and the depression of GLR-1-mediated behaviours. Surprisingly, hypoxia-inducible factor (HIF)-1, the canonical substrate of EGL-9, is not required for this effect. Instead, EGL-9 interacts with the Mint orthologue LIN-10, a mediator of GLR-1 membrane recycling, to promote LIN-10 subcellular localization in an oxygen-dependent manner. The observed effects of hypoxia and egl-9 mutations require the activity of the proline-directed CDK-5 kinase and the CDK-5 phosphorylation sites on LIN-10, suggesting that EGL-9 and CDK-5 compete in an oxygen-dependent manner to regulate LIN-10 activity and thus GLR-1 trafficking. Our findings demonstrate a novel mechanism by which neurons sense and respond to hypoxia.
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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.