? ? Environmental Stress Signaling and Cellular Consequences (ESSCC) result from exposure to environmental xenobiotics, drugs, oxidants, radiation, ischemia/reperfusion, and nutritional imbalances. Despite the diversity of environmental stresses, there is a commonality in the responses of numerous cell types to these insults. Because environmentally and/or xenobiotically mediated diseases and the majority of other diseases incorporate cell injury, death, carcinogenesis, and a diminished capacity for cellular repair and regeneration in their pathology, the need for scientists trained in ESSCC is critical. The objective of the ESSCC Training Program is to train new scientists to address mechanisms of ESSCC and to translate findings into the development of interventions or novel therapeutics that prevent or diminish cell injury, death, and carcinogenesis, and/or promote repair and regeneration. In addition, new scientists entering this area of research will be able to use recently developed genomic, proteomic, and bioinformatic technologies to elucidate mechanisms of ESSCC. The trainees will come from various backgrounds that encompass chemical, physical, and biomedical sciences and will be integrated into the interdepartmental didactic and research ESSCC Training Program. It is anticipated that the training afforded by the ESSCC Program will result in new scientists that address the consequences of exposures to environmental xenobiotics. The primary principle uniting the mentors of the ESSCC Training Program is the universal role of environmental stress signaling and cellular consequences in environmentally and xenobiotically mediated diseases and other diverse diseases, and the belief that cells from different organ systems exhibit many common responses to diverse insults and stresses. It is viewed that advances in understanding ESSCC and training future scientists in ESSCC can be accomplished more quickly through integration of ESSCC efforts of scientists across classic departments and disciplines. ? ? ?
| Saunders, Janet E; Beeson, Craig C; Schnellmann, Rick G (2013) Characterization of functionally distinct mitochondrial subpopulations. J Bioenerg Biomembr 45:87-99 |
| Peterson, Yuri K; Cameron, Robert B; Wills, Lauren P et al. (2013) ?2-Adrenoceptor agonists in the regulation of mitochondrial biogenesis. Bioorg Med Chem Lett 23:5376-81 |
| Heffernan-Stroud, Linda A; Obeid, Lina M (2013) Sphingosine kinase 1 in cancer. Adv Cancer Res 117:201-35 |
| Smith, Matthew A; Schnellmann, Rick G (2012) Mitochondrial calpain 10 is degraded by Lon protease after oxidant injury. Arch Biochem Biophys 517:144-52 |
| Smith, Matthew A; Schnellmann, Rick G (2012) Calpains, mitochondria, and apoptosis. Cardiovasc Res 96:32-7 |
| Smith, Matthew A; Covington, Marisa D; Schnellmann, Rick G (2012) Loss of calpain 10 causes mitochondrial dysfunction during chronic hyperglycemia. Arch Biochem Biophys 523:161-8 |
| Funk, Jason A; Schnellmann, Rick G (2012) Persistent disruption of mitochondrial homeostasis after acute kidney injury. Am J Physiol Renal Physiol 302:F853-64 |
| Smith, Matthew A; McInnes, Campbell; Whitaker, Ryan M et al. (2012) Calpain 10 homology modeling with CYGAK and increased lipophilicity leads to greater potency and efficacy in cells. ACS Chem Biol 7:1410-9 |
| Mullen, Thomas D; Obeid, Lina M (2012) Ceramide and apoptosis: exploring the enigmatic connections between sphingolipid metabolism and programmed cell death. Anticancer Agents Med Chem 12:340-63 |
| Mullen, Thomas D; Hannun, Yusuf A; Obeid, Lina M (2012) Ceramide synthases at the centre of sphingolipid metabolism and biology. Biochem J 441:789-802 |
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