ArticleProceedings of the National Academy of Sciences of the United States of America2011
Human sweet taste receptor mediates acid-induced sweetness of miraculin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Pre-treatment with creatinine alters the perceived bitterness-sweetness balance of L-histidine in young Japanese female participants.Chemical senses · 2026Article
- Feeding the estrobolome with sweet prebiotics?Frontiers in nutrition · 2026Review
- The non-synthetic sweeteners, miraculin and mogroside V, but not stevia, disrupt the intestinal epithelial barrier function through a sweet taste receptor-dependent mechanism.Scientific reports · 2025Article
- Comprehensive New Insights into Sweet Taste Transmission Mechanisms and Detection Methods.Foods (Basel, Switzerland) · 2025Review
- Miraculin Can Contribute to a Reduction in Inflammatory Biomarkers and Cachexia in Malnourished Patients with Cancer and Taste Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Miracle Fruit, a Potential Taste-modifier to Improve Food Preferences: A Review.Current nutrition reports · 2024Review
- Intrinsic Molecular Proton Sensitivity Underlies GPR4 Effects on Retrotrapezoid Nucleus Neuronal Activation and COThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Tongue-on-a-Chip: Parallel Recording of Sweet and Bitter Receptor Responses to Sequential Injections of Pure and Mixed Sweeteners.Journal of agricultural and food chemistry · 2024Article
- Mechanisms and Functions of Sweet Reception in Oral and Extraoral Organs.International journal of molecular sciences · 2024Review
- Neuroscience of taste: unlocking the human taste code.BMC neuroscience · 2024Review
- Article
- Pharmacology of TAS1R2/TAS1R3 Receptors and Sweet Taste.Handbook of experimental pharmacology · 2022Article
- Protein music of enhanced musicality by music style guided exploration of diverse amino acid properties.Heliyon · 2021Article
- The accumulation of recombinant miraculin is independent of fruit size in tomato.Plant biotechnology (Tokyo, Japan) · 2021Article
- New Insight Into the Structure-Activity Relationship of Sweet-Tasting Proteins: Protein Sector and Its Role for Sweet Properties.Frontiers in nutrition · 2021Article
- The Chromosome-Level Genome of Miracle Fruit (Frontiers in plant science · 2021Article
- Miracle Berry as a Potential Supplement in the Control of Metabolic Risk Factors in Cancer.Antioxidants (Basel, Switzerland) · 2020Review
- Alteration, Reduction and Taste Loss: Main Causes and Potential Implications on Dietary Habits.Nutrients · 2020Review
- Flavor Alterations Associated with Miracle Fruit and Gymnema sylvestre.Chemical senses · 2018Article
- Intracellular acidification is required for full activation of the sweet taste receptor by miraculin.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Miraculin (MCL) is a homodimeric protein isolated from the red berries of Richadella dulcifica. MCL, although flat in taste at neutral pH, has taste-modifying activity to convert sour stimuli to sweetness. Once MCL is held on the tongue, strong sweetness is sensed over 1 h each time we taste a sour solution. Nevertheless, no molecular mechanism underlying the taste-modifying activity has been clarified. In this study, we succeeded in quantitatively evaluating the acid-induced sweetness of MCL using a cell-based assay system and found that MCL activated hT1R2-hT1R3 pH-dependently as the pH decreased from 6.5 to 4.8, and that the receptor activation occurred every time an acid solution was applied. Although MCL per se is sensory-inactive at pH 6.7 or higher, it suppressed the response of hT1R2-hT1R3 to other sweeteners at neutral pH and enhanced the response at weakly acidic pH. Using human/mouse chimeric receptors and molecular modeling, we revealed that the amino-terminal domain of hT1R2 is required for the response to MCL. Our data suggest that MCL binds hT1R2-hT1R3 as an antagonist at neutral pH and functionally changes into an agonist at acidic pH, and we conclude this may cause its taste-modifying activity.
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