NOW PUBLISHED
Special issue on
Nutrigenomics
Edited by L.R. Ferguson, A.N. Shelling, D. Lauren, J.A. Heyes, W.C. McNabb
The scope of Mutation Research: Molecular and Fundamental Mechanisms broadly encompasses all aspects of research that address the
detection of mutations, the mechanisms by which mutations in genes and chromosomes arise, and the modulation of mutagenesis by mutation
avoidance pathways such as DNA repair, cell ... click here for full Aims & Scope
The scope of Mutation Research: Molecular and Fundamental Mechanisms broadly encompasses all aspects of research that address the
detection of mutations, the mechanisms by which mutations in genes and chromosomes arise, and the modulation of mutagenesis by mutation
avoidance pathways such as DNA repair, cell cycle control and apoptosis. It includes the role of genetic variation in the genesis and
manifestation of mutations, ranging from the variable manner in which xenobiotics are metabolized to variations in the capacity of cells
to replicate and repair damaged DNA. It also includes the contributions of these mechanisms, when perturbed, to animal disease models
and to human disease, with particular emphasis on carcinogenic mechanisms. Chromosome stability is paramount for maintaining cellular
homeostasis. Therefore, the Journal will publish articles on the genesis of aneuploidy and isodisomy, including the roles played by cell
cycle checkpoints, spindle microtubules, centrosomes and kinetocore proteins, and agents that might disrupt them. Since isodisomy can
occur as a consequence of recombination, all aspects of homologous recombination and non-homologous end joining are appropriate. Submission
of appropriate epidemiological studies as well as consequences, including methods for high throughput SNP detection, DNA microarrays
and proteomic approaches, are welcome. The broader scope of the journal is a reflection of the rapid advances in the field of mutation
research and the recognition that cellular responses to DNA damage, including cell cycle checkpoint arrest and apoptosis, cannot be dissociated
from the immediate mechanisms by which DNA is damaged and repaired.
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