| First Author | Wintermantel TM | Year | 2004 |
| Journal | Horm Metab Res | Volume | 36 |
| Issue | 6 | Pages | 387-91 |
| PubMed ID | 15241729 | Mgi Jnum | J:91827 |
| Mgi Id | MGI:3050910 | Doi | 10.1055/s-2004-814567 |
| Citation | Wintermantel TM, et al. (2004) Genetic dissection of corticosteroid receptor function in mice. Horm Metab Res 36(6):387-91 |
| abstractText | Functional genomic technologies, including artificial chromosome-based transgenesis and conditional gene targeting, allowed us to generate mouse models harboring genes with loss-of-function mutations, gain-of-function mutations, spatially and/or temporally restricted mutations, tissue-specific mutations, and function-selective mutations. This kind of 'allelic series' for corticosteroid receptors in mouse models provides a very useful resource for the molecular understanding of corticosteroid function in vivo. These models will also support the identification of steroid receptor target genes in order to define a steroid signaling cascade in molecular terms. They provide opportunities for the identification of compounds that regulate steroid receptors in a tissue-specific and function-selective manner. For example, selective glucocorticoid receptor modulators preventing receptor dimerization and DNA binding can be expected to reduce osteoporotic and/or diabetogenic side effects, but to display partial or full anti-inflammatory potential. Thus, these mouse models will help to evaluate distinct steroid receptor functions for therapeutic intervention. |
