The goal of this project is to define how basic cellular mechanisms suppress, activate and execute the process of apoptosis or programmed cell death. Apoptosis is a fundamental component of virtually all aspects of biology, being critical for both developmental and cellular homeostasis in all multi-cellular organisms. Extensive studies worldwide have now implicated either excess or impaired apoptosis in numerous human diseases including cancer, AIDS, autoimmune diseases, sepsis, as well as toxic responses to environmental agents. Additionally, many of the therapies used for the treatment of cancer work by the activation of inherent cellular apoptotic programs.

Project Start
Project End
Budget Start
Budget End
Support Year
18
Fiscal Year
2013
Total Cost
$895,765
Indirect Cost
City
State
Country
Zip Code
Cain, Derek W; Cidlowski, John A (2015) Specificity and sensitivity of glucocorticoid signaling in health and disease. Best Pract Res Clin Endocrinol Metab 29:545-56
Franco, Rodrigo; Bortner, Carl D; Schmitz, Ingo et al. (2014) Glutathione depletion regulates both extrinsic and intrinsic apoptotic signaling cascades independent from multidrug resistance protein 1. Apoptosis 19:117-34
Kadmiel, Mahita; Cidlowski, John A (2013) Glucocorticoid receptor signaling in health and disease. Trends Pharmacol Sci 34:518-30
Busillo, John M; Cidlowski, John A (2013) The five Rs of glucocorticoid action during inflammation: ready, reinforce, repress, resolve, and restore. Trends Endocrinol Metab 24:109-19
Cao, Yun; Bender, Ingrid K; Konstantinidis, Athanasios K et al. (2013) Glucocorticoid receptor translational isoforms underlie maturational stage-specific glucocorticoid sensitivities of dendritic cells in mice and humans. Blood 121:1553-62
Whirledge, Shannon; Cidlowski, John A (2013) Estradiol antagonism of glucocorticoid-induced GILZ expression in human uterine epithelial cells and murine uterus. Endocrinology 154:499-510
Ramamoorthy, Sivapriya; Cidlowski, John A (2013) Ligand-induced repression of the glucocorticoid receptor gene is mediated by an NCoR1 repression complex formed by long-range chromatin interactions with intragenic glucocorticoid response elements. Mol Cell Biol 33:1711-22
Ramamoorthy, Sivapriya; Cidlowski, John A (2013) Exploring the molecular mechanisms of glucocorticoid receptor action from sensitivity to resistance. Endocr Dev 24:41-56
Revollo, Javier R; Oakley, Robert H; Lu, Nick Z et al. (2013) HES1 is a master regulator of glucocorticoid receptor-dependent gene expression. Sci Signal 6:ra103
Whirledge, Shannon; Xu, Xiaojiang; Cidlowski, John A (2013) Global gene expression analysis in human uterine epithelial cells defines new targets of glucocorticoid and estradiol antagonism. Biol Reprod 89:66

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