Jun 15, 2016 · The present study was designed to investigate whether inhibiting JNK activity would partially restore the PI3K/Akt signaling pathway and protect against myocardial I/R injury in diabetic rats, and to explore the effect of intervention with salvianolic acid A (Sal A).

The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway and c-Jun N-terminal kinase (JNK) pathway are responsible for regulating a variety of cellular processes including cell growth, migration, invasion and apoptosis.

Recent studies have demonstrated that diabetes impairs the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway, while insulin resistance syndrome has been associated with alterations of this pathway in diabetic rats after ischemia/reperfusion (I/R), and activation of C-jun N-terminal kinase (JNK) is involved.

In this review, we first summarized the functional characteristics, signal transduction and activation mechanisms of the PI3K/Akt and JNK pathways, and then discussed the dual roles of JNK pathway in apoptosis and tumor development.

In the present study, we describe a novel signaling axis of the c-Jun NH2 kinase (JNK) and signal transducer and activator of transcription 3 (Stat3) and its involvement in As 3+ -induced Akt activation in human bronchial epithelial cells.

May 22, 2017 · Schematic representation of the regulation of p21 by 3-AWA. 3-AWA induces Par-4 and stimulates ER stress-mediated activation of JNK. The simultaneous inhibition of AKT by 3-AWA favors a cross...

One potential mechanism responsible for attenuated Akt phosphorylation is activation of JNK, which has been implicated in the development of complications associated with type 2 diabetes .

20 hours ago · JNK inhibitor and BML-260 treatment together produced similar effects on Dex-induced myotube atrophy compared to SP600125 or BML-260 alone (Appendix Fig. S6). ... Chen WR, and Xing D A pathway from JNK through decreased ERK and Akt activities for FOXO3a nuclear translocation in response to UV irradiation J Cell Physiol 2012 227 1168-1178. Crossref.

Nov 28, 2003 · The pro-survival effects of Akt are likely to be mediated in part through its regulation of the c-Jun N-terminal kinase (JNK) signaling pathway. The JNK signaling pathway is a mitogen activated protein kinase (MAPK) cascade in which a MAPKKK activates a MAPKK, which then activates a MAPK, JNK (12, 13). MAPKKKs for the JNK signaling pathway ...

We demonstrated that COP up-regulated phase II antioxidant enzymes NAD (P)H/quinone oxidoreductase 1 (NQO1) through activating the nuclear factor erythroid-2 related factor 2 (Nrf2). Moreover, as the upstream signalings of Nrf2, the protein kinase B (Akt) and c-Jun NH2-terminal kinase (JNK) signalings were also induced by COP.