( use data combined with the findings in...)ESR1 Gene Expression in Oncology and Metabolic Diseases Using the ASCENTATM System ,,, Target Validation and Identification of Novel Disease Indications

use data, combined with the findings in the ASCENTA System, indicate that regulation of ESR1 in obesity and diabetes is worth further investigation and may provide clues about additional disease application areas for this drug target. The ESR1 expression changes found by the ASCENTA System in obese and diabetic human liver and skeletal muscle tissue samples are indeed novel findings.

For many gene targets, it is often appropriate to investigate their expression metrics within the broadened context of a gene family or a biological pathway to which they belong. Such investigations can often reveal novel expression relationships between members of gene families or pathway interactors which may provide more insight into the mechanism of human disease and reveal additional related targets to be considered as biomarkers or drug candidates themselves.

Gene Logic has curated and annotated members of "drug-able" gene families and key regulatory biological pathways and provides these as compiled collections of genes in the ASCENTA System. The gene families include many commonly investigated groups such as G-protein coupled receptors and protein kinases. Biological pathways are from the Kyoto Encyclopedia of Genes and Genomes (KEGG) and BioCarta. Since ESR1 is a member of the Nuclear Hormone Receptor (NHR) family, one can select the NHR family in the Gene Family Browser, quickly review detailed information about NHRs with links to other information sources, view a compiled list of curated family members, and obtain a Diff/X report of differential gene expression of NHRs in all or any one of the five major therapeutic areas (Figure 5, left panel). Detailed information about two pathways (of which ESR1 is a member) is easily accessed through the Pathway Browser (Figure 5, right panel). These two pathways are titled "CARM1 and Regulation of the Estrogen Receptor" and "Pelp1 Modulation of Estrogen Receptor Activity". C
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