ArticleBiochemistry2009
Conserved rhodopsin intradiscal structural motifs mediate stabilization: effects of zinc.
Article in Biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Conformational signatures of native ligand and pharmacochaperone binding in rhodopsin.Structure (London, England : 1993) · 2026Article
- Zinc in eye health, retinal biology and disease.Progress in retinal and eye research · 2025Review
- Putative retina metal/metalloid-binding proteins: molecular functions, biological processes and retina disease associations.Metallomics : integrated biometal science · 2024Article
- Effect of Trace Metal Ions on the Conformational Stability of the Visual Photoreceptor Rhodopsin.International journal of molecular sciences · 2023Article
- Native Mass Spectrometry Reveals the Simultaneous Binding of Lipids and Zinc to Rhodopsin.International journal of mass spectrometry · 2021Article
- A Multi-Omics Approach Identifies Key Regulatory Pathways Induced by Long-Term Zinc Supplementation in Human Primary Retinal Pigment Epithelium.Nutrients · 2020Article
- Zinc Protects Oxidative Stress-Induced RPE Death by Reducing Mitochondrial Damage and Preventing Lysosome Rupture.Oxidative medicine and cellular longevity · 2017Article
- A reduced zinc diet or zinc transporter 3 knockout attenuate light induced zinc accumulation and retinal degeneration.Experimental eye research · 2013Article
- Insights from the analysis of conserved motifs and permitted amino acid exchanges in the human, the fly and the worm GPCR clusters.Bioinformation · 2011Article
- Light-induced photoreceptor and RPE degeneration involve zinc toxicity and are attenuated by pyruvate, nicotinamide, or cyclic light.Molecular vision · 2010Article
- Allosteric Modulation of G Protein Coupled Receptors by Cytoplasmic, Transmembrane and Extracellular Ligands.Pharmaceuticals (Basel, Switzerland) · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Retinitis pigmentosa (RP), a neurodegenerative disorder, can arise from single point mutations in rhodopsin, leading to a cascade of protein instability, misfolding, aggregation, rod cell death, retinal degeneration, and ultimately blindness. Divalent cations, such as zinc and copper, have allosteric effects on misfolded aggregates of comparable neurodegenerative disorders including Alzheimer disease, prion diseases, and ALS. We report that two structurally conserved low-affinity zinc coordination motifs, located among a cluster of RP mutations in the intradiscal loop region, mediate dose-dependent rhodopsin destabilization. Disruption of native interactions involving histidines 100 and 195, through site-directed mutagenesis or exogenous zinc coordination, results in significant loss of receptor stability. Furthermore, chelation with EDTA stabilizes the structure of both wild-type rhodopsin and the most prevalent rhodopsin RP mutation, P(23)H. These interactions suggest that homeostatic regulation of trace metal concentrations in the rod outer segment of the retina may be important both physiologically and for an important cluster of RP mutations. Furthermore, with a growing awareness of allosteric zinc binding domains on a diverse range of GPCRs, such principles may apply to many other receptors and their associated diseases.
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Registered trials
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