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Published online 12 March 2004

Nucleic Acids Research, 2004, Vol. 32, No. 5 1731-1737
© 2004 Oxford University Press

Bioinformatical assay of human gene morbidity

Fyodor A. Kondrashov, Aleksey Y. Ogurtsov and Alexey S. Kondrashov*

National Center for Biotechnology Information, National Institutes of Health, 38a Center Drive, 6S602, Bethesda, MD 20892, USA

*To whom correspondence should be addressed. Tel: +1 301 435 8944; Fax: +1 301 480 2290; Email: kondrashov{at}ncbi.nlm.nih.gov

Only a fraction of eukaryotic genes affect the phenotype drastically. We compared 18 parameters in 1273 human morbid genes, known to cause diseases, and in the remaining 16 580 unambiguous human genes. Morbid genes evolve more slowly, have wider phylogenetic distributions, are more similar to essential genes of Drosophila melanogaster, code for longer proteins containing more alanine and glycine and less histidine, lysine and methionine, possess larger numbers of longer introns with more accurate splicing signals and have higher and broader expressions. These differences make it possible to classify as non-morbid 34% of human genes with unknown morbidity, when only 5% of known morbid genes are incorrectly classified as non-morbid. This classification can help to identify disease-causing genes among multiple candidates.


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