Review
Copyright ©The Author(s) 2015.
World J Gastroenterol. Mar 28, 2015; 21(12): 3492-3498
Published online Mar 28, 2015. doi: 10.3748/wjg.v21.i12.3492
Figure 1
Figure 1 Long-chain acyl-CoA synthetases induce apoptotic cell death via the c-Jun N-terminal kinase pathway. JNK can be activated via phosphorylation by increased ceramide which can be induced by ACSLs that subsequently activate caspase 3, leading to apoptotic cell death. This shows that ACSLs may induce apoptotic cell death via the JNK pathway. In addition, anti-apoptotic proteins such as cFLIP, which is downregulated by ACSLs, may inhibit the activation of JNK. ACSL: Long-chain acyl-CoA synthetase; cFLIP: Cellular Fas associated death domain-like interleukin-1β converting enzyme inhibitory protein; JNK: c-Jun N-terminal kinase; TRAIL: Tumor necrosis factor-related apoptosis inducing ligand; TRAIL-R1: Tumor necrosis factor-related apoptosis inducing ligand receptor 1.