ArticleProtein science : a publication of the Protein Society2011
Probing the self-association, intermolecular contacts, and folding propensity of amelogenin.
Article in Protein science : a publication of the Protein Society, 2011. 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, 27 citations in OpenAlex.
- Mechanisms of Enamel Mineralization Guided by Amelogenin Nanoribbons.Journal of dental research · 2021Review
- Controls of nature: Secondary, tertiary, and quaternary structure of the enamel protein amelogenin in solution and on hydroxyapatite.Journal of structural biology · 2020Review
- Progression of Self-Assembly of Amelogenin Protein Supramolecular Structures in Simulated Enamel Fluid.Biomacromolecules · 2018Article
- Interactions of amelogenin with phospholipids.Biopolymers · 2015Article
- Improved protocol to purify untagged amelogenin - Application to murine amelogenin containing the equivalent P70→T point mutation observed in human amelogenesis imperfecta.Protein expression and purification · 2015Article
- Structural adaptation of tooth enamel protein amelogenin in the presence of SDS micelles.Biopolymers · 2014Article
- A solution NMR investigation into the impaired self-assembly properties of two murine amelogenins containing the point mutations T21→I or P41→T.Archives of biochemistry and biophysics · 2013Article
- Why do proteins aggregate? "Intrinsically insoluble proteins" and "dark mediators" revealed by studies on "insoluble proteins" solubilized in pure water.F1000Research · 2013Review
- Protein-mediated enamel mineralization.Frontiers in bioscience (Landmark edition) · 2012Review
- Use of human amelogenin in molecular encapsulation for the design of pH responsive microparticles.BMC biotechnology · 2012Article
- Amelogenin and Enamel Biomimetics.Journal of materials chemistry. BArticle
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Amelogenins are an intrinsically disordered protein family that plays a major role in the development of tooth enamel, one of the most highly mineralized materials in nature. Monomeric porcine amelogenin possesses random coil and residual secondary structures, but it is not known which sequence regions would be conformationally attractive to potential enamel matrix targets such as other amelogenins (self-assembly), other matrix proteins, cell surfaces, or biominerals. To address this further, we investigated recombinant porcine amelogenin (rP172) using "solvent engineering" techniques to simultaneously promote native-like structure and induce amelogenin oligomerization in a manner that allows identification of intermolecular contacts between amelogenin molecules. We discovered that in the presence of 2,2,2-trifluoroethanol (TFE) significant folding transitions and stabilization occurred primarily within the N- and C-termini, while the polyproline Type II central domain was largely resistant to conformational transitions. Seven Pro residues (P2, P127, P130, P139, P154, P157, P162) exhibited conformational response to TFE, and this indicates these Pro residues act as folding enhancers in rP172. The remaining Pro residues resisted TFE perturbations and thus act as conformational stabilizers. We also noted that TFE induced rP172 self-association via the formation of intermolecular contacts involving P4-H6, V19-P33, and E40-T58 regions of the N-terminus. Collectively, these results confirm that the N- and C-termini of amelogenin are conformationally responsive and represent potential interactive sites for amelogenin-target interactions during enamel matrix mineralization. Conversely, the Pro, Gln central domain is resistant to folding and this may have important functional significance for amelogenin.
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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.