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. Author manuscript; available in PMC: 2013 May 27.
Published in final edited form as: Kidney Int. 2011 Nov;80(9):905–907. doi: 10.1038/ki.2011.263

Figure 2.

Figure 2

BAD signaling. This diagram shows possible alternative regulatory pathways that result in phosphorylation and inactivation of BAD resulting in enhanced cell survival. PGE2 initiates an increase in cAMP that can activate PKA and EPAC, both of which can phosphorylate BAD on Ser-155 by different signaling pathways. RSK, which is downstream of EPAC can also be activated by PKC independently of cAMP. Other signaling pathways can influence BAD activity by phosphorylating serine residues other than Ser-155 (e.g., Ser 112, Ser-136). For example, AKT can be activated by phosphoinositide 3-kinase (PI3K), heat shock protein 90 (HSP90) and heat shock protein 27 (HSP 27). Akt phosphorylates BAD on Ser-136 which promotes inactivation by cytosolic sequestration. BAD binds to and inactivates anti-apoptotic proteins at the mitochondria resulting in release of cytochrome C and activation of the caspase cascade leading to cell death. Phosphorylation of BAD prevents this binding and thus leads to cell survival.