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Enamel biomineralization: Solution- and solid-state NMR studies of a natural protein-mineral interface


EMSL Project ID
47735

Abstract

The protein amelogenin is the central protein that controls the formation of dental enamel, the hardest tissue in the human body. The protein orchestrates the nucleation, growth, and organization of enamel formation (amelogenesis) through the formation of large quaternary structures called nanospheres, consisting of 20-100 monomers. The structure and function of full-length amelogenin and LRAP, the latter a splice variant of amelogenin that contains only the charged N- and C- termini, are the focus of our four-year, NIH funded investigations. Solution-state structural studies are being conducted on full-length amelogen, two naturally occurring mutants, and LRAP, with an emphasis on characterizing structure under the variety of conditions found during enamel growth. Solid-state quantitative structural and orientation studies of the protein bound to hydroxyapatite are focused on LRAP, as its smaller size allows easy incorporation of selective isotopic labels which enable the determination of site specific, molecular level protein structure, protein-surface interactions and dynamics. Structural changes observed in solution or in the solid-state will then be correlated to differences in function.

Project Details

Start Date
2012-12-05
End Date
2013-11-13
Status
Closed

Team

Principal Investigator

Garry Buchko
Institution
Pacific Northwest National Laboratory

Team Members

Junxia Lu
Institution
Pacific Northwest National Laboratory

Wendy Shaw
Institution
Pacific Northwest National Laboratory

Barbara Tarasevich
Institution
Pacific Northwest National Laboratory

Related Publications

A solution NMR investigation into the impaired self-assembly properties of two murine amelogenins containing the point mutations T21→I or P41→T

Buchko GW, G Lin, BJ Tarasevich, and WJ Shaw. 2013. "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 537(2):217-224. doi:10.1016/j.abb.2013.07.015