Lin Wang
Clemson University
11 Papers
31 Citations
Lin Wang is an academic researcher from Clemson University. The author has contributed to research in topics: Chemistry & Missense mutation. The author has an hindex of 11, co-authored 11 publications.
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Papers
pKa predictions for proteins, RNAs, and DNAs with the Gaussian dielectric function using DelPhi pKa
Lin Wang,Lin Li,Emil Alexov +2 more
TL;DR: Investigations showed that predictions for most of buried mutant residues of SNase could be improved by using higher dielectric constant values and an option to generate different hydrogen positions also improves pKa predictions for buried carboxyl residues.
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DelPhiPKa web server: predicting pKa of proteins, RNAs and DNAs
Lin Wang,Min Zhang,Emil Alexov +2 more
TL;DR: In this paper, a new pKa prediction web server is released, which implements DelPhi Gaussian dielectric function to calculate electrostatic potentials generated by charges of biomolecules.
Predicting folding free energy changes upon single point mutations
TL;DR: An approach that predicts the free energy change upon single point mutation by utilizing the 3D structure of the wild-type protein based on variation of the molecular mechanics Generalized Born method, scaled with optimized parameters (sMMGB) and utilizing specific model of unfolded state.
Developing hybrid approaches to predict pKa values of ionizable groups
TL;DR: A hybrid approach is reported that first predicts the titratable groups whose ionization is expected to cause large conformational changes, termed “problematic” residues, and then applies a special protocol on them, while the rest of the pKas are predicted with rigid backbone approach as implemented in multi‐conformation continuum electrostatics (MCCE) method.
A Y328C missense mutation in spermine synthase causes a mild form of Snyder–Robinson syndrome
Zhe Zhang,Joy Norris,Vera M. Kalscheuer,Tim Wood,Lin Wang,Charles E. Schwartz,Emil Alexov,Hilde Van Esch +7 more
TL;DR: The biochemical and in silico studies confirm the p.Y328C mutation in SMS is responsible for the patients having a mild form of SRS and reveal yet another molecular mechanism resulting in a non-functional SMS causing SRS.