ArticleScience advances2024
Mechanisms underlying modulation of human GlyRα3 by Zn
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Human GlyRα2 pore dynamics in gating and inhibition.Structure (London, England : 1993) · 2026Article
- Extracellular KNature communications · 2026Article
- Zinc Overload in Microvessels Contributes to Blood-Brain Barrier Disruption by Activating the JAK2 Pathway After Cerebral Ischemia/Reperfusion.CNS neuroscience & therapeutics · 2026Article
- Structure of a pH-sensitive pentameric ligand-gated ion channel from the Sarcoptes scabies mite.Nature communications · 2026Article
- Structural insights into the progressive recovery of α7 nicotinic acetylcholine receptor from nicotine-induced desensitization.Science advances · 2025Article
- Molecular determinants of cesium- and glycine-dependent glycine receptor activation.Scientific reports · 2025Article
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.
Funding
Abstract
Glycine receptors (GlyRs) regulate motor control and pain processing in the central nervous system through inhibitory synaptic signaling. The subtype GlyRα3 expressed in nociceptive sensory neurons of the spinal dorsal horn is a key regulator of physiological pain perception. Disruption of spinal glycinergic inhibition is associated with chronic inflammatory pain states, making GlyRα3 an attractive target for pain treatment. GlyRα3 activity is modulated by numerous endogenous and exogenous ligands that consequently affect pain sensitization. To understand the mechanism of two such endogenous modulators, Zn
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What Socratic 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 Socratic graph.