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Human MAPK10 Protein expressed in Wheat germ - ABIN1310260
Prause, Christensen, Billestrup, Mandrup-Poulsen: JNK1 protects against glucolipotoxicity-mediated beta-cell apoptosis. dans PLoS ONE 2014
multiple residues on the non-receptor-binding side of arrestin-3 are crucial for JNK3 activation
identification of an intricate SDF-1alpha-induced signaling cascade that involves eNOS, JNK3, and MKP7and enhances endothelial migration
Significantly, we show that introduction of mapk10 mutations into ret heterozygotes enhanced the ENS deficit, supporting MAPK10 as a Hirschsprung disease (HSCR) susceptibility locus. Our studies demonstrate that ret heterozygous zebrafish is a sensitized model, with many significant advantages over existing murine models, to explore the pathophysiology and complex genetics of HSCR.
phosphorylation rate of JNK3 at Thr-221 by MKK7 is two orders of magnitude faster than the corresponding phosphorylation of Tyr-223 by MKK4 with or without arrestin-3
Mapk10 expression was regulated by miR27a-3p in nasopharyngeal carcinoma.Mapk10 gene was down-regulated in the nasopharyngeal carcinoma cells.
Peptide mini-scaffold facilitates JNK3 activation in cells.
Study found that JNK3 levels are increased in brain tissue and CSF from patients with Alzheimer disease and CSF levels could reflect the rate of cognitive decline
Data indicate that tetra-substituted pyridinylimidazoles were designed as dual inhibitors of c-Jun N-terminal kinase (JNK) 3 and p38alpha mitogen-activated protein (MAP) kinase, and both kinases may be involved in the progression of Huntington's disease.
JNK3 is required for the antiapoptotic effects of exendin 4
analysis of the unique mechanisms by which JNK1beta1 is regulated
Mitogen-activated protein kinase 10 JNK3 alpha (JNK3apha2)binds to both domains of arrestin-3.
miR-29b mRNA, MAPK10 protein expression, and ATG9A protein expression are closely related to chemosensitivity of ovarian carcinoma.
Subtle structural mechanisms for allosteric signaling between the peptide-binding site and activation loop of human JNK3.
reduced JNK3 activity has potentially deleterious effects on neuronal function via altered regulation of a set of post-synaptic proteins.
Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 activity in cell by dominant-negative arrestin-3 mutant.
[review] This review focuses on delineating the role of scaffold proteins, especially that of JNK3 as a target, on the regulation of JNK signaling in neurons.
Arrestin-3 acts as a "true" scaffold, facilitating JNK3alpha2 phosphorylation by bringing it and MAP kinase kinase (MKK)4 together.
The results suggest the possible involvement of CaMKII and JNK3 in soman-induced long-term neurotoxicity.
results suggest that MAPK10 may have a proapoptotic function and could function as a tumor-suppressor gene in chromophobe renal cell carcinoma
JNK1, JNK2, and JNK3 are involved in P-glycoprotein-mediated multidrug resistance of hepatocellular carcinoma cells.
Shares a promoter region with the tightly linked gene encoding Fas-associated phosphatase-1.
interaction of free arrestins with JNK3 and Mdm2 and their ability to regulate subcellular localization of these proteins may play an important role in the survival of photoreceptors and other neurons
Arrestin in all conformations binds JNK3 comparably, whereas Mdm2 preferentially binds cone arrestin 'frozen' in the basal state.
Together these data indicate that ONA induces APP expression and that gamma-secretase cleavage of APP releases AICD, which upregulates JNK3 leading to RGC death. This pathway may be a novel target for neuronal protection in optic neuropathies and other forms of neurotrauma.
JNK1 and/or JNK3 are promising targets for the prevention of cell death and inflammation during epileptogenesis.
Conversely, treatment with LY294002 (a selective inhibitor of Akt1) reversed the effects of quercetin. In conclusion, these findings highlight the important role of quercetin in protecting against cognitive deficits and inhibiting neuronal apoptosis via the Akt signaling pathway. We believe that quercetin might prove to be a useful therapeutic component in treating cerebral I/R diseases in the near future.
JNK3 therefore provides a mechanism that contributes to homeostatic regulation of energy balance in response to metabolic stress.
Genetic inhibition of JNK pathway in vivo by Jnk3 knockout results in amelioration of spinal muscular atrophy phenotype
Rotenone induces dopamine neuron death through a series of sequential events including microtubule destabilization, JNK3 activation, VMAT2 inhibition, accumulation of cytosolic dopamine, and generation of ROS.
the data on anxiety, exploration and learning indicate that JNK1 ko mice displayed a stronger explorative behaviour and that knockout of JNK2 or JNK3
JNK3 signaling is a major early pathway triggering retinal ganglion cell (RGC) death after axonal injury and may directly link axon injury to transcriptional activity that controls RGC death.
Deletion of JNK3 from Alzheimer (AD) mice results in a dramatic reduction in Abeta42 levels, overall plaque loads, and increased neuronal number and improved cognition, revealing AD as a metabolic disease under tight control by JNK3.
Mice deficient for neuron-specific isoform JNK3 have altered behavioural rhythms, with longer free-running period and compromised phase shifts to light.
Overall, our results show the transcriptional regulation of the MAPK pathway and the essential role of JNK in Japanese Encephalitis Virus-induced apoptosis in neuroblastoma cells.
This study indicated that the activation of PI3K/AKT pathway in hippocampus because of the increase in pik3cb transcription and that this mechanism is specifically related to the lack of Jnk3.
JNK2 and JNK3 are critically involved in stress-induced deficit of contextual fear, while JNK1 mainly regulates baseline learning in this behavioral task.
Results demonstrate that p75NTR-mediated activation of JNK3 is required for up-regulation of TACE, which promotes receptor proteolysis, leading to prolonged activation of JNK3 and subsequent apoptosis in sympathetic neurons.
Data show that neuritogenesis is delayed by lack of JNK2 and JNK3, but not JNK1.
JNK3 in neurons has a critical role in ischemic apoptosis
JNKs can mediate death independently of c-Jun
Stimulation of ceramide biosynthesis seems to be under control of JNK3 signaling
MyD88-5 is distinct from other MyD88s in that MyD88-5 is preferentially expressed in neurons, colocalizes in part with mitochondria and JNK3, and regulates neuronal death.
the AtMKK2-AtMPK10 MAPK module regulates leaf venation complexity by altering polar auxin transport efficiency
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This protein is a neuronal-specific form of c-Jun N-terminal kinases (JNKs). Through its phosphorylation and nuclear localization, this kinase plays regulatory roles in the signaling pathways during neuronal apoptosis. Beta-arrestin 2, a receptor-regulated MAP kinase scaffold protein, is found to interact with, and stimulate the phosphorylation of this kinase by MAP kinase kinase 4 (MKK4). Cyclin-dependent kianse 5 can phosphorylate, and inhibit the activity of this kinase, which may be important in preventing neuronal apoptosis. Four alternatively spliced transcript variants encoding distinct isoforms have been reported.
mitogen-activated protein kinase 10
, MAP kinase 10
, MAPK 10
, Stress activated protein kinase beta
, c-Jun N-terminal kinase 3
, stress-activated protein kinase JNK3
, JNK3 alpha protein kinase
, MAP kinase p49 3F12
, stress activated protein kinase beta
, stress-activated protein kinase 1b
, JNK3 beta1 protein kinase
, JNK3 beta2 protein kinase
, SAPK/Erk/kinase 2
, mitogen activated protein kinase 10