Soc. Extrinsic apoptosis pathway is one of the signal pathways which may trigger the process of programmed cell death namely cell apoptosis. 72(2), 379–86. Overview of Extrinsic Apoptosis Pathway Apoptosis is known as a physiological process of cell deletion and is also a process of programmed cell death, resulting in morphological change and DNA fragmentation.
Constitutive activation of extracellular signal regulated kinase (ERK)-Jun NH2-terminal kinase (JNK) signaling commonly occurs in tumors. In addition, activity of the C-Jun NH 2-terminal kinases (JNK) pathway and p38 mitogen-activated protein kinase (MAPK) pathway was evaluated by Western blot. ... Bax, and an elevation in the anti-apoptotic protein, Bcl-xL, potentially mediated by down-regulation of ASK1-JNK pathway.
Trans. JNK signaling regulates a wide range of cellular processes, including cell proliferation, differentiation, survival, apoptosis, and inflammation. 40(1), 85–9. However, the apoptotic mechanism of ERK-JNK signaling in cancer is … The activation of ERK promotes cell proliferation, whereas that of JNK induces cell apoptosis. Davies C, Tournier C (2012) Exploring the function of the JNK (c-Jun N-terminal kinase) signalling pathway in physiological and pathological processes to design novel therapeutic strategies. Dysregulation of JNK pathway is associated with a wide range of immune disorders and cancer. 3.6.
Biochem. Melatonin Protects Cardiomyocytes from Apoptosis Induced by Hypoxia and High-Glucose/High-Fat Treatment via the JNK-Mediated Apoptosis Pathway. Cancer Res. Apoptosis requires the activation of multiple signaling cascades, including the c-Jun N-terminal kinase (JNK) pathway, which has been reported to stimulate apoptosis in porcine GCs . The c-Jun N-terminal kinases (JNKs), with its members JNK1, JNK2, and JNK3, is a subfamily of (MAPK) mitogen-activated protein kinases.
Similarly, JNK pathway inhibitor SP600125 (10 μM) also inhibited cell growth and invasion and induced apoptosis.
Chen F (2012) JNK-induced apoptosis, compensatory growth, and cancer stem cells. In addition, experiments in nude mice showed that PM inhibited tumor formation through Ca 2+ /CaMKII/JNK signaling pathway. To gain insight into the underlying molecular mechanism, we considered a role of the JNK pathway since it is activated during stress-induced apoptosis in Drosophila and plays a role for the induction of Dpp and Wg in apoptotic cells (Ryoo et al., 2004; Perez-Garijo et al., 2009). JNK promotes apoptosis through two different mechanisms. We further examined levels of JNK and related apoptotic proteins in H9c2 cells treated with the JNK activator anisomycin under hypoxia in conjunction with high-glucose/high-fat insult. Since JNK is activated by phosphorylation at c-Jun N-terminal, we measured the level of phosphorylated JNK by Western blot.
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