Recombinant Mouse Mitogen-activated protein kinase 10 (Mapk10)

Product Details

Abbreviation
Mapk10
Purity
>85% (SDS-PAGE)
Target Names
Mapk10
Uniprot NO.
Species
Mus musculus (Mouse)
Source
Yeast
Expression Region
1-464
Target Protein Sequence
MSLHFLYYCS EPTLDVKIAF CQGFDKHVDV SSIAKHYNMS KSKVDNQFYS VEVGDSTFTV LKRYQNLKPI GSGAQGIVCA AYDAVLDRNV AIKKLSRPFQ NQTHAKRAYR ELVLMKCVNH KNIISLLNVF TPQKTLEEFQ DVYLVMELMD ANLCQVIQME LDHERMSYLL YQMLCGIKHL HSAGIIHRDL KPSNIVVKSD CTLKILDFGL ARTAGTSFMM TPYVVTRYYR APEVILGMGY KENVDIWSVG CIMGEMVRHK ILFPGRSYID QWNKVIEQLG TPCPEFMKKL QPTVRNYVEN RPKYAGLTFP KLFPDSLFPA DSEHNKLKAS QARDLLSKML VIDPVKRISV DDALQHPYIN VWYDPAEVEA PPPQIYDKQL DEREHTIEEW KELIYKEVMN SEEKTKNGVV KSQPSPSGAA VNSSESLPPS SAVNDISSMS TDQTLASDTD SSLEASAGPL GCCR
Note: The complete sequence may include tag sequence, target protein sequence, linker sequence and extra sequence that is translated with the protein sequence for the purpose(s) of secretion, stability, solubility, etc.
If the exact amino acid sequence of this recombinant protein is critical to your application, please explicitly request the full and complete sequence of this protein before ordering.
Protein Length
full length protein
Tag Info
N-terminal His-tagged/Tag-Free
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Storage
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Customer Reviews and Q&A

 Customer Reviews

Target Background

Function(From Uniprot)
Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity. Plays regulatory roles in the signaling pathways during neuronal apoptosis. Phosphorylates the neuronal microtubule regulator STMN2. Acts in the regulation of the amyloid-beta precursor protein/APP signaling during neuronal differentiation by phosphorylating APP. Participates also in neurite growth in spiral ganglion neurons. Phosphorylates the CLOCK-ARNTL/BMAL1 heterodimer and plays a role in the photic regulation of the circadian clock. Phosphorylates JUND and this phosphorylation is inhibited in the presence of MEN1.
Gene References into Functions
  1. JNK3 therefore provides a mechanism that contributes to homeostatic regulation of energy balance in response to metabolic stress. PMID:26910012
  2. Genetic inhibition of JNK pathway in vivo by Jnk3 knockout results in amelioration of spinal muscular atrophy phenotype PMID:26423457
  3. 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. PMID:25496994
  4. the data on anxiety, exploration and learning indicate that JNK1 ko mice displayed a stronger explorative behaviour and that knockout of JNK2 or JNK3 PMID:23428746
  5. 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. PMID:22353563
  6. 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. PMID:22958823
  7. Mice deficient for neuron-specific isoform JNK3 have altered behavioural rhythms, with longer free-running period and compromised phase shifts to light. PMID:22441692
  8. 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. PMID:21320173
  9. 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. PMID:21255018
  10. JNK2 and JNK3 are critically involved in stress-induced deficit of contextual fear, while JNK1 mainly regulates baseline learning in this behavioral task. PMID:20926661
  11. 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. PMID:20421303
  12. Data show that neuritogenesis is delayed by lack of JNK2 and JNK3, but not JNK1. PMID:20534829
  13. JNK3 in neurons has a critical role in ischemic apoptosis PMID:14657393
  14. JNKs can mediate death independently of c-Jun PMID:15528206
  15. 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 PMID:16737965
  16. Stimulation of ceramide biosynthesis seems to be under control of JNK3 signaling PMID:17609208
  17. 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. PMID:17724133
  18. JNK2/3 double deficiency blocks death due to retinoblastoma loss in both the PNS and CNS and In the medulla region of the hindbrain in the CNS, JNK2/3 deficiency blocks p53 activation. PMID:17984095
  19. data identify JNK3 as a critical mediator of pathogenic Htt (polyQ-Htt)toxicity and provide a molecular basis for polyQ-Htt-induced inhibition of fast axonal transport. PMID:19525941
  20. The activation of SAPK/JNK in basket cell "pinceaux" may be a consequence of altered functionality of Purkinje cells and may represent an attempt of basket cells of synaptic remodeling. PMID:19703431

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Subcellular Location
Cytoplasm. Membrane; Lipid-anchor. Nucleus. Mitochondrion.
Protein Families
Protein kinase superfamily, CMGC Ser/Thr protein kinase family, MAP kinase subfamily
Tissue Specificity
Brain (at protein level). Expressed specifically in neurons of the hippocampus, cortex, cerebellum, brainstem, and spinal cord. Seems to be also found in testis, and very weakly in the heart.
Database Links

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