RESUMEN
Copper is an essential micronutrient for all biological systems. Multiple proteins require one or more atoms of copper for proper structure and function, but excess of copper is toxic. To prevent the consequences of copper deficiency and overload, living organisms have evolved molecular mechanisms that regulate its uptake, intracellular traffic, storage, and efflux. Underlying some of the cellular responses to variations in copper levels are changes in the expression of genes encoding molecular components of copper metabolism. In recent years, genome-scale expression analysis in several eukaryotic models has allowed the identification of copper-responsive genes involved in copper homeostasis. Characterization of the transcriptional changes in response to varying copper levels include both genes directly involved in copper homeostasis and genes involved in different cellular process that, even though they are not directly connected to copper metabolism, change their expression during the cellular adaptation to copper availability. Evaluation of these gene expression patterns could aid in the identification of biologically relevant markers to monitor copper status in humans.