The overall goal of the Molecular Endocrinology Group in the Laboratory of Signal Transduction is to understand how cells and tissues respond to environmental stress. Insights into stress signaling pathways can aid in the understanding of human disease processes and their therapeutic treatment. Our research group has focused its research efforts on the actions of glucocorticoids, a primary stress response hormone released following the activation of the hypothalamic pituitary adrenal axis. Chronic evaluation of glucocorticoids due to prolonged stress and/or chronic therapeutic intervention with glucocorticoids has numerous detrimental actions on human health and studying their actions and signaling pathways is critical to the mission of NIEHS. We seek to understand how glucocorticoids signal in a cell specific manner in order to provide insights and discoveries concerning their actions on cell growth, differentiation and cell death. Glucocorticoids are steroid hormones derived from the metabolic conversion of cholesterol in the adrenal gland. They are necessary for life as judged from hormone deprivation studies and more recent deletion of the glucocorticoid receptor gene in mice. These hormones regulate numerous aspects of physiology including glucose homeostasis, protein metabolism, skeletal growth, connective tissue metabolism, respiratory function, immune surveillance and components of human behavior. This diversity of actions has made glucocorticoids attractive for therapeutic development and, as a class of compounds, they are among the most prescribed drugs in the world. They remain a primary treatment for the environmental disease, asthma, as well as a host of other inflammatory conditions in humans.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Intramural Research (Z01)
Project #
1Z01ES090057-08
Application #
6840741
Study Section
(LST)
Project Start
Project End
Budget Start
Budget End
Support Year
8
Fiscal Year
2003
Total Cost
Indirect Cost
Name
U.S. National Inst of Environ Hlth Scis
Department
Type
DUNS #
City
State
Country
United States
Zip Code
Min, Jungki; Perera, Lalith; Krahn, Juno M et al. (2018) Probing Dominant Negative Behavior of Glucocorticoid Receptor ? through a Hybrid Structural and Biochemical Approach. Mol Cell Biol :
Jewell, Christine M; Cidlowski, John A (2007) Molecular evidence for a link between the N363S glucocorticoid receptor polymorphism and altered gene expression. J Clin Endocrinol Metab 92:3268-77
Lu, Nick Z; Collins, Jennifer B; Grissom, Sherry F et al. (2007) Selective regulation of bone cell apoptosis by translational isoforms of the glucocorticoid receptor. Mol Cell Biol 27:7143-60
Lewis-Tuffin, Laura J; Jewell, Christine M; Bienstock, Rachelle J et al. (2007) Human glucocorticoid receptor beta binds RU-486 and is transcriptionally active. Mol Cell Biol 27:2266-82
Duma, Danielle; Jewell, Christine M; Cidlowski, John A (2006) Multiple glucocorticoid receptor isoforms and mechanisms of post-translational modification. J Steroid Biochem Mol Biol 102:11-21
Tliba, Omar; Cidlowski, John A; Amrani, Yassine (2006) CD38 expression is insensitive to steroid action in cells treated with tumor necrosis factor-alpha and interferon-gamma by a mechanism involving the up-regulation of the glucocorticoid receptor beta isoform. Mol Pharmacol 69:588-96
Lu, Nick Z; Cidlowski, John A (2006) Glucocorticoid receptor isoforms generate transcription specificity. Trends Cell Biol 16:301-7
Lewis-Tuffin, Laura J; Cidlowski, John A (2006) The physiology of human glucocorticoid receptor beta (hGRbeta) and glucocorticoid resistance. Ann N Y Acad Sci 1069:1-9
Franco, Rodrigo; Cidlowski, John A (2006) SLCO/OATP-like transport of glutathione in FasL-induced apoptosis: glutathione efflux is coupled to an organic anion exchange and is necessary for the progression of the execution phase of apoptosis. J Biol Chem 281:29542-57
Panayiotidis, M I; Bortner, C D; Cidlowski, J A (2006) On the mechanism of ionic regulation of apoptosis: would the Na+/K+-ATPase please stand up? Acta Physiol (Oxf) 187:205-15

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