Publication List

@article{Furney2006,
title = {Differences in the evolutionary history of disease genes affected by dominant or recessive mutations.},
author = {Furney, Simon J and Albà, M Mar and López-Bigas, Núria},
url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1534034&tool=pmcentrez&rendertype=abstract},
issn = {1471-2164},
year = {2006},
date = {2006-01-01},
journal = {BMC genomics},
volume = {7},
pages = {165},
abstract = {Global analyses of human disease genes by computational methods have yielded important advances in the understanding of human diseases. Generally these studies have treated the group of disease genes uniformly, thus ignoring the type of disease-causing mutations (dominant or recessive). In this report we present a comprehensive study of the evolutionary history of autosomal disease genes separated by mode of inheritance.},
keywords = {Amino Acid, Animals, Caenorhabditis elegans, Caenorhabditis elegans: genetics, Computational Biology, Conserved Sequence, Dominant, Essential, Evolution, Genes, Genetic, Genetic Diseases, Genetic Structures, Humans, Inborn, Inborn: classification, Inborn: genetics, Mice, Molecular, Mutation, Pan troglodytes, Pan troglodytes: genetics, Recessive, Selection, Sequence Homology}
}

@article{Huang2004,
title = {Evolutionary conservation and selection of human disease gene orthologs in the rat and mouse genomes.},
author = {Huang, Hui and Winter, Eitan E and Wang, Huajun and Weinstock, Keith G and Xing, Heming and Goodstadt, Leo and Stenson, Peter D and Cooper, David N and Smith, Douglas and Albà, M Mar and Ponting, Chris P and Fechtel, Kim},
url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=463309&tool=pmcentrez&rendertype=abstract},
issn = {1465-6914},
year = {2004},
date = {2004-01-01},
journal = {Genome biology},
volume = {5},
number = {7},
pages = {R47},
abstract = {Model organisms have contributed substantially to our understanding of the etiology of human disease as well as having assisted with the development of new treatment modalities. The availability of the human, mouse and, most recently, the rat genome sequences now permit the comprehensive investigation of the rodent orthologs of genes associated with human disease. Here, we investigate whether human disease genes differ significantly from their rodent orthologs with respect to their overall levels of conservation and their rates of evolutionary change.},
keywords = {Amino Acid, Amino Acid: genetics, Animal, Animals, Chromosome Mapping, Chromosome Mapping: methods, Conserved Sequence, Conserved Sequence: genetics, Disease Models, Evolution, Fishes, Fishes: genetics, Fungal, Fungal: genetics, Genes, Genes: genetics, Genes: physiology, Genetic, Genetic Diseases, Genome, Helminth, Helminth: genetics, human, Humans, Inborn, Inborn: genetics, Inborn: physiopathology, Insect, Insect: genetics, Mice, Molecular, Mutagenesis, Mutagenesis: genetics, Nucleic Acid, Nucleotides, Nucleotides: genetics, Point Mutation, Point Mutation: genetics, Rats, Repetitive Sequences, Selection, Sequence Homology, Trinucleotide Repeat Expansion, Trinucleotide Repeat Expansion: genetics}
}