Abstract

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.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Investigator-Initiated Intramural Research Projects (ZIA)
Project #
1ZIAES090079-18
Application #
8734120
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
18
Fiscal Year
2013
Total Cost
$895,765
Indirect Cost

  Institution

Name
National Institute of Environmental Health Sciences
Department
Type
DUNS #
City
State
Country
Zip Code

  Publications

Whirledge, Shannon D; Kisanga, Edwina P; Oakley, Robert H et al. (2018) Neonatal Genistein Exposure and Glucocorticoid Signaling in the Adult Mouse Uterus. Environ Health Perspect 126:047002
Olivares-Morales, Mauricio Javier; De La Fuente, Marjorie Katherine; Dubois-Camacho, Karen et al. (2018) Glucocorticoids Impair Phagocytosis and Inflammatory Response Against Crohn's Disease-Associated Adherent-Invasive Escherichia coli. Front Immunol 9:1026
Santen, Richard J; Jewell, Christine M; Yue, Wei et al. (2018) Glucocorticoid receptor mutations and hypersensitivity to endogenous and exogenous glucocorticoids. J Clin Endocrinol Metab :
Oakley, Robert H; Ramamoorthy, Sivapriya; Foley, Julie F et al. (2018) Glucocorticoid receptor isoform-specific regulation of development, circadian rhythm, and inflammation in mice. FASEB J :fj201701153R
Cain, Derek W; Cidlowski, John A (2017) Immune regulation by glucocorticoids. Nat Rev Immunol 17:233-247
Oakley, Robert H; Busillo, John M; Cidlowski, John A (2017) Cross-talk between the glucocorticoid receptor and MyoD family inhibitor domain-containing protein provides a new mechanism for generating tissue-specific responses to glucocorticoids. J Biol Chem 292:5825-5844
Whirledge, Shannon; Cidlowski, John A (2017) Glucocorticoids and Reproduction: Traffic Control on the Road to Reproduction. Trends Endocrinol Metab 28:399-415
Busada, Jonathan T; Cidlowski, John A (2017) Mechanisms of Glucocorticoid Action During Development. Curr Top Dev Biol 125:147-170
Regan Anderson, Tarah M; Ma, Shi Hong; Raj, Ganesh V et al. (2016) Breast Tumor Kinase (Brk/PTK6) Is Induced by HIF, Glucocorticoid Receptor, and PELP1-Mediated Stress Signaling in Triple-Negative Breast Cancer. Cancer Res 76:1653-63
Quinn, Matthew A; Cidlowski, John A (2016) Endogenous hepatic glucocorticoid receptor signaling coordinates sex-biased inflammatory gene expression. FASEB J 30:971-82

Showing the most recent 10 out of 39 publications