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- W2068165232 endingPage "925" @default.
- W2068165232 startingPage "918" @default.
- W2068165232 abstract "Glucocorticoids regulate a wide range of systems in vertebrate organisms, and their effects are mediated by the glucocorticoid receptor (GR). The responsiveness to glucocorticoids differs largely between individuals. Resistance to glucocorticoids is an important medical problem, since it limits the efficacy of glucocorticoids when they are used to treat immune-related diseases like asthma and rheumatoid arthritis. Glucocorticoid resistance also contributes to the pathogenesis of other diseases, like major depression because of the decreased negative feedback on the hypothalamic pituitary adrenal axis. In this review, we present the zebrafish as an excellent in vivo model system to study glucocorticoid resistance. First, the zebrafish is the only non-primate animal model in which a β-isoform of GR occurs, which is a splice variant with dominant-negative activity. Zebrafish are easily genetically modified, so the expression of GRβ can be varied, creating an in vivo model for GRβ-induced glucocorticoid resistance. Second, by performing a forward-genetic screen using the glucocorticoid-induced decrease in POMC expression in the pituitary gland as a readout, several zebrafish mutants have been obtained which appear to be resistant to glucocorticoid treatment. We present here two types of in vivo models for studying glucocorticoid resistance, that will be used to study the molecular mechanism of glucocorticoid signaling and resistance. Finally these models will be used to screen for small molecules that can alleviate glucocorticoid resistance." @default.
- W2068165232 created "2016-06-24" @default.
- W2068165232 creator A5003398229 @default.
- W2068165232 creator A5022892166 @default.
- W2068165232 creator A5065083412 @default.
- W2068165232 date "2010-12-01" @default.
- W2068165232 modified "2023-09-26" @default.
- W2068165232 title "The zebrafish as an in vivo model system for glucocorticoid resistance" @default.
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