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抗Rat (Rattus) MAPK10 抗体:
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抗Mouse (Murine) MAPK10 抗体:
Human Monoclonal MAPK10 Primary Antibody for IHC, ELISA - ABIN966522
Gupta, Barrett, Whitmarsh, Cavanagh, Sluss, Dérijard, Davis: Selective interaction of JNK protein kinase isoforms with transcription factors. in The EMBO journal 1996
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Human Monoclonal MAPK10 Primary Antibody for ELISA, WB - ABIN966521
Cuenda: Mitogen-activated protein kinase kinase 4 (MKK4). in The international journal of biochemistry & cell biology 2000
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Human Monoclonal MAPK10 Primary Antibody for ICC, ELISA - ABIN1724701
Kinet, Bernard, Mongellaz, Perreau, Goldman, Taylor: gp120-mediated induction of the MAPK cascade is dependent on the activation state of CD4(+) lymphocytes. in Blood 2002
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Bat Polyclonal MAPK10 Primary Antibody for WB - ABIN611114
Deaglio, Morra, Mallone, Ausiello, Prager, Garbarino, Dianzani, Stockinger, Malavasi: Human CD38 (ADP-ribosyl cyclase) is a counter-receptor of CD31, an Ig superfamily member. in Journal of immunology (Baltimore, Md. : 1950) 1998
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Human Polyclonal MAPK10 Primary Antibody for IHC (p), WB - ABIN391727
Yoshida, Harada, Nagai, Fukino, Teramoto, Emi: Head-to-head juxtaposition of Fas-associated phosphatase-1 (FAP-1) and c-Jun NH2-terminal kinase 3 (JNK3) genes: genomic structure and seven polymorphisms of the FAP-1 gene. in Journal of human genetics 2002
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Human Polyclonal MAPK10 Primary Antibody for ICC, IF - ABIN446845
Salvucci, Ohnuki, Maric, Hou, Li, Yoon, Segarra, Eberhart, Acker-Palmer, Tosato: EphrinB2 controls vessel pruning through STAT1-JNK3 signalling. in Nature communications 2015
multiple residues on the non-receptor-binding side of arrestin-3 (显示 ARRB2 抗体) are crucial for JNK3 activation
identification of an intricate SDF-1alpha-induced signaling cascade that involves eNOS (显示 NOS3 抗体), JNK3, and MKP7and enhances endothelial migration
Significantly, we show that introduction of mapk10 mutations into ret (显示 RET 抗体) heterozygotes enhanced the ENS deficit, supporting MAPK10 as a Hirschsprung disease (HSCR (显示 EDNRB 抗体)) susceptibility locus. Our studies demonstrate that ret (显示 RET 抗体) heterozygous zebrafish is a sensitized model, with many significant advantages over existing murine models, to explore the pathophysiology and complex genetics of HSCR (显示 EDNRB 抗体).
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 (显示 CSF2 抗体) from patients with Alzheimer disease and CSF (显示 CSF2 抗体) 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 (显示 MAPK14 抗体) mitogen-activated protein (MAP) kinase (显示 MAPK1 抗体), 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 (显示 ARRB2 抗体).
miR (显示 MLXIP 抗体)-29b mRNA, MAPK10 protein expression, and ATG9A (显示 ATG9A 抗体) 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 (显示 ARRB2 抗体) mutant.
Conversely, treatment with LY294002 (a selective inhibitor of Akt1 (显示 AKT1 抗体)) 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 (显示 AKT1 抗体) 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 (显示 MAPK8 抗体) 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 (显示 ROS1 抗体).
the data on anxiety, exploration and learning indicate that JNK1 (显示 MAPK8 抗体) ko mice displayed a stronger explorative behaviour and that knockout of JNK2 (显示 MAPK9 抗体) 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 (显示 MAPK1 抗体) pathway and the essential role of JNK (显示 MAPK8 抗体) in Japanese Encephalitis Virus-induced apoptosis in neuroblastoma (显示 ARHGEF16 抗体) cells.
This study indicated that the activation of PI3K/AKT (显示 AKT1 抗体) pathway in hippocampus because of the increase in pik3cb transcription and that this mechanism is specifically related to the lack of Jnk3.
the AtMKK2 (显示 MAP2K2 抗体)-AtMPK10 MAPK (显示 MAPK1 抗体) 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