Computational Mutation Project

Shenzhen, Taiwan

Computational Mutation Project

Shenzhen, Taiwan
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Yan S.,Guangxi Academy of science | Wu G.,Computational Mutation Project
Annals of Biomedical Engineering | Year: 2010

Quantification of mutation capacity within a protein could be a way to model the mutation relationship not only because history might not leave many cues on the causes for mutations but also the evolved protein might no longer be subject to previous mutation causes. Randomness should play a constant role in engineering mutations in proteins because randomness suggests the maximal probability of occurrence by which a protein would be constructed with the least time and energy to meet the speed of rapidly changing environments. Since 1999, we have developed three approaches for quantifying of randomness of protein by which each amino acid has three numeric values. In this study, we model our three random numeric values in each amino acid with occurrence and non-occurrence of mutation, which are classified as unity and zero, using a 3-6-1 feedforward backpropagation neural network to predict the mutation positions in H5N1 neuraminidases. The results show that the neural network can capture the mutation relationship as measured by prediction sensitivity, specificity, and total correct rate. With the help of translation probability between RNA codes and mutated amino acids, we predict the would-be-mutated amino acids at predicted mutation positions. © 2010 Biomedical Engineering Society.


Yan S.,Guangxi Academy of science | Wu G.,Computational Mutation Project
Biomedical and Environmental Sciences | Year: 2011

Objective: To determine if global warming has an impact on the evolution of hemagglutinins from influenza A viruses, because both global warming and influenza pandemics/epidemics threaten the world. 4 706 hemagglutinins from influenza A viruses sampled from 1956 to 2009 were converted to a time-series to show their evolutionary process and compared with the global, northern hemisphere and southern hemisphere temperatures, to determine if their trends run in similar or opposite directions. Point-to-point comparisons between temperature and quantified hemagglutinins were performed for all species and for the major prevailing species. The comparisons show that the trends for both hemagglutinin evolution and temperature change run in a similar direction. Global warming has a consistent and progressive impact on the hemagglutinin evolution of influenza A viruses. © 2011 The Editorial Board of Biomedical and Environmental Sciences.


Yan S.,Guangxi Academy of science | Wu G.,Computational Mutation Project
Computer Methods in Biomechanics and Biomedical Engineering | Year: 2010

The phenotype expression in X-linked adrenoleukodystrophy is one of the most intriguing issues of the disease, because there is no general correlation between the type of ABCD1 gene mutation and the clinical phenotype. In this study, we use the cross-impact analysis to build a descriptively quantitative relationship between mutant adrenoleukodystrophy protein and classification of adrenoleukodystrophy with the amino-acid distribution probability, which is a quantitative measure sensitive to mutation. Then we determine the probability that the adrenoleukodystrophy can be classified under mutations with the help of a Bayesian equation. © 2010 Taylor & Francis.


Yan S.,Guangxi Academy of science | Li Z.,Guangxi Academy of science | Wu G.,Computational Mutation Project
Protein and Peptide Letters | Year: 2010

The understanding of evolutionary mechanism is important, and equally important is to describe the evolutionary process. If so, we would know where the biological evolution will go. At species level, we would know whether and when a species will extinct or be prosperous. At protein level, we would know when a protein family will mutate more. In our previous study, we explored the possibility of using the differential equation to describe the evolution of protein family from influenza A virus based on the assumption that the mutation process is the exchange of entropy between protein family and its environment. In this study, we use the analytical solution of system of differential equations to fit the evolution of matrix protein 1 family from influenza A virus. Because the evolutionary process goes along the time course, it can be described by differential equation. The results show that the evolution of a protein family can be fitted by the analytical solution. With the obtained fitted parameters, we may predict the evolution of matrix protein 1 family from influenza A virus. Our model would be the first step towards the systematical modeling of biological evolution and paves the way for further modeling. © 2010 Bentham Science Publishers Ltd.


Yan S.,Guangxi Academy of science | Wu G.,Computational Mutation Project
Molecular Diversity | Year: 2010

A way to study the mutation pattern is to convert a 20-letter protein sequence into a scalar protein sequence, because the 20-letter protein sequence is neither vector nor scalar while a promising way to study patterns is in numerical domain. In this study, we use the amino-acid pair predictability to convert α-galactosidase A with its 137 mutations into scalar sequences, and analyse which amino-acid pairs are more sensitive to mutation. Our results show that the unpredictable amino-acid pairs are more sensitive to mutation, and the mutation trend is to narrow the difference between predicted and actual frequency of amino-acid pairs. © 2009 Springer Science+Business Media B.V.


Yan S.,Guangxi Academy of science | Wu G.,Computational Mutation Project
2010 4th International Conference on Bioinformatics and Biomedical Engineering, iCBBE 2010 | Year: 2010

Cystathionine β-synthase deficiency is an inborn error of metabolism that is biochemically characterized by severe hyperhomocysteinemia and homocystinuria. Numerous cystathionine β-synthase mutants have so far been found in patients with cystathionine β-synthase deficiency. In this study, we use the cross-impact analysis to model the cystathionine β-synthase mutants with their clinical endpoints, and found the probability that the severity of cystathionine β-synthase deficiency can be determined under mutations. Our results show that a patient with cystathionine β-synthase deficiency has about one third chance of being defined severity when a new mutation is found in human cystathionine β-synthase. © 2010 IEEE.

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