title: Cyclooxygenase-2 in the kidney: good, BAD, or both?
abstract: Hypertonic stress in the kidney inner medulla is common, yet inner medullary cells adapt to limit cell death. Küper et al. have identified a cell-survival response by which increased cyclooxygenase-2 (COX-2) stimulates a prostaglandin E(2) (PGE(2))/protein kinase A (PKA)-mediated inactivation of the pro-apoptotic protein BAD. However, the PGE(2)/PKA pathway is not the only means to inactivate BAD and limit cell death. This Commentary shows a broader picture of this pathway to examine the kidney's BAD options.
authors: Renal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA.
authors: S
authors: S
authors: Russ Price
authors: Renal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA. Electronic address: janet.klein@emory.edu.
authors: Janet D
authors: JD
authors: Klein
mesh_terms: D000818:Animals; D017209:Apoptosis; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D004847:Epithelial Cells / Q000201:enzymology*; D007679:Kidney Medulla / Q000201:enzymology*; D051025:bcl-Associated Death Protein / Q000378:metabolism*
chemical_list: C494820:Bad protein, mouse; D051025:bcl-Associated Death Protein; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2