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multiple residues on the non-receptor-binding side of arrestin-3 (show ARRB2 ELISA Kits) are crucial for JNK3 activation
identification of an intricate SDF-1alpha-induced signaling cascade that involves eNOS (show NOS3 ELISA Kits), JNK3, and MKP7and enhances endothelial migration
Significantly, we show that introduction of mapk10 mutations into ret (show RET ELISA Kits) heterozygotes enhanced the ENS deficit, supporting MAPK10 as a Hirschsprung disease (HSCR (show EDNRB ELISA Kits)) susceptibility locus. Our studies demonstrate that ret (show RET ELISA Kits) heterozygous zebrafish is a sensitized model, with many significant advantages over existing murine models, to explore the pathophysiology and complex genetics of HSCR (show EDNRB ELISA Kits).
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 (show CSF2 ELISA Kits) from patients with Alzheimer disease and CSF (show CSF2 ELISA Kits) 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 (show MAPK14 ELISA Kits) mitogen-activated protein (MAP) kinase (show MAPK1 ELISA Kits), and both kinases may be involved in the progression of Huntington's disease.
JNK3 is required for the antiapoptotic effects of exendin 4
Mitogen-activated protein kinase 10 JNK3 alpha (JNK3apha2)binds to both domains of arrestin-3 (show ARRB2 ELISA Kits).
miR (show MLXIP ELISA Kits)-29b mRNA, MAPK10 protein expression, and ATG9A (show ATG9A ELISA Kits) 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 (show ARRB2 ELISA Kits) mutant.
Conversely, treatment with LY294002 (a selective inhibitor of Akt1 (show AKT1 ELISA Kits)) 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 (show AKT1 ELISA Kits) 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 (show MAPK8 ELISA Kits) 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 (show Slc18a2 ELISA Kits) inhibition, accumulation of cytosolic dopamine, and generation of ROS (show ROS1 ELISA Kits).
the data on anxiety, exploration and learning indicate that JNK1 (show MAPK8 ELISA Kits) ko mice displayed a stronger explorative behaviour and that knockout of JNK2 (show MAPK9 ELISA Kits) 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 (show MAPK1 ELISA Kits) pathway and the essential role of JNK (show MAPK8 ELISA Kits) in Japanese Encephalitis Virus-induced apoptosis in neuroblastoma (show ARHGEF16 ELISA Kits) cells.
This study indicated that the activation of PI3K/AKT (show AKT1 ELISA Kits) pathway in hippocampus because of the increase in pik3cb transcription and that this mechanism is specifically related to the lack of Jnk3.
the AtMKK2 (show MAP2K2 ELISA Kits)-AtMPK10 MAPK (show MAPK1 ELISA Kits) 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