JNK
- Mitochondrial dysfunction triggers a catabolic response in chondrocytes via ROS-mediated activation of the JNK/AP1 pathway
Summary: Mitochondrial dysfunction triggers the expression of osteoarthritis-related catabolic genes in human chondrocytes through a mechanism that involves reactive oxygen species-dependent activation of the JNK/AP1 pathway.
- Wnt7b signalling through Frizzled-7 receptor promotes dendrite development by coactivating CaMKII and JNK
Summary: Fz7 functions as a Wnt7b receptor to modulate dendrite development and complexity by coactivating the CaMKII and JNK signalling cascades.
- Stress-activated MAPKs and CRM1 regulate the subcellular localization of Net1A to control cell motility and invasion
Summary: Stress-activated MAPKs and the nuclear exportin CRM1 regulate translocation of the RhoA subfamily GEF Net1A from the nucleus to the cytoplasm to control RhoA signaling, cell motility and extracellular matrix invasion.
- An initial phase of JNK activation inhibits cell death early in the endoplasmic reticulum stress response
Summary: Activation of JNK by ER stress kinetically precedes activation of XBP1 by IRE1α. JNK-dependent induction of several inhibitors of apoptosis inhibits apoptosis early in the ER stress response.
- KCNK1 inhibits osteoclastogenesis by blocking the Ca2+ oscillation and JNK–NFATc1 signaling axis
Summary: The inwardly rectifying K+ channel KCNK1 negatively regulates osteoclast differentiation.
- JNK2 controls fragmentation of the Golgi complex and the G2/M transition through phosphorylation of GRASP65
Summary: JNK2-mediated phosphorylation of GRASP65 at Ser277 has a crucial role in the G2-specific separation of the Golgi stacks that is required for the G2/M transition.