Apoptosis Signal Regulating Kinase 1 (ASK1) and transforming growth factor B-activated kinase 1 (TAK1) in Inflammatory Renal Disease

Inflammation is a feature of acute and chronic renal disease. This thesis examined the upstream pathways by which the stress-activated proteins, p38 and JNK, become activated to cause inflammatory damage in the kidney. Using a combination of drug-based and genetic approaches in models of kidney disease, these studies identified two upstream enzymes in this pathway that exert opposing effects upon the stress-activated proteins. One of these enzymes, called apoptosis signal-regulating kinase 1, is identified as a therapeutic target in the treatment of inflammatory kidney disease.