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Inducible and constitutive transcription factors in the mammalian nervous system: control of gene expression by Jun, Fos and Krox, and CREB/ATF proteins
JNK and p38 stresskinases — degenerative effectors of signal-transduction-cascades in the nervous system
The c-Jun transcription factor – bipotential mediator of neuronal death, survival and regeneration
JNK1 phosphorylation of SCG10 determines microtubule dynamics and axodendritic length
This work affinity purified JNK-interacting proteins from brain and demonstrated that inhibition of cytoplasmic JNK and expression of SCG10-62A/73A both inhibited fluorescent tubulin recovery after photobleaching suggest that JNK1 is responsible for regulation ofSCG10 depolymerizing activity and neurite elongation during brain development.
The bottleneck of JNK signaling: molecular and functional characteristics of MKK4 and MKK7.
Lasting N-Terminal Phosphorylation of c-Jun and Activation of c-Jun N-Terminal Kinases after Neuronal Injury
It is demonstrated that lasting c-Jun S73 phosphorylation and JNK activity are part of neuronal stress response after neurodegenerative disorders in the adult mammalian brain with Fas-ligand as a putative apoptotic effector.
CD95 Ligand (Fas-L/APO-1L) and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Mediate Ischemia-Induced Apoptosis in Neurons
An involvement of CD95 ligand and TRAIL in the pathophysiology of postischemic neurodegeneration is suggested and alternative strategies for the treatment of cardiovascular brain disease are offered.
AP-1 proteins in the adult brain: facts and fiction about effectors of neuroprotection and neurodegeneration
The multiple molecular interfunctions which are involved in the shift from the physiological role to degenerative effects of the Jun/JNK-axis such as cell type-specific expression and intracellular localization of scaffold proteins and upstream activators, antagonistic phosphatases, interaction with other kinase systems, or the activation of transcription factors competing for binding to JNK proteins and AP-1 DNA elements are summarized.
Specific pathophysiological functions of JNK isoforms in the brain
Surprisingly, the deletion of a single JNK isoform did not attenuate the immunocytochemical signal of phosphorylated c‐Jun irrespective on the experimental set‐up.
c-Jun N-Terminal Protein Kinase (JNK) 2/3 Is Specifically Activated by Stress, Mediating c-Jun Activation, in the Presence of Constitutive JNK1 Activity in Cerebellar Neurons
It is demonstrated that neuronal stress induces strong activation of JNK2/3 in the presence of constitutively and highly active JNK1, and this JNK 2/3 activity selectively targets c-Jun, which is isolated from constitutive J NK1 activity.