Genetic dissection of gluco- and mineralocorticoid receptor function
in mice
E. F. Greiner, S. Berger, and G. Sch�tz
Department of Molecular Biology of the Cell I, German
Cancer Research Center, Im Neuenheimer Feld 280, 60120 Heidelberg, Germany
Abstract: Nuclear hormone receptors function to transduce hormonal
signals into transcriptional responses by controlling the activity of
specific target genes. These target genes comprise a genetic network
whose coordinate activity defines the physiological responses to hormonal
signals. Dissecting nuclear hormone receptor functions in vivo by gene
inactivation and transgenic strategies represents an invaluable and
powerful approach to increase our knowledge of these genetic networks
and their physiological functions. Glucocorticoids and mineralocorticoids
are involved in numerous physiological processes important to maintain
metabolic, cardiovascular, central nervous, and immune system homeostasis.
Germline and somatic gene targeting as well as an increased dosage of
the glucocorticoid receptor (GR) allows the characterization of the
various functions and molecular modes of action of this receptor. Most
of the effects of the GR are mediated via activation and repression
of gene expression. To separate activating from repressing functions
of the GR, a point mutation was introduced which allowed us to characterize
and distinguish functions dependent on GR binding to DNA from those
mediated by protein/protein interaction. Cell/tissue-specific mutations
of the gluco- and mineralocorticoid receptor is the basis for the evaluation
of their cell-specific functions, including the characterization of
target genes of the receptors in order to describe their specific effects
on different targets.
*Report from a SCOPE/IUPAC project: Implication of
Endocrine Active Substances for Human and Wildlife (J. Miyamoto and
J.Burger, editors). Other reports are published in this issue,
pp. 1617-2615.
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