c-Jun, Recombinant, Human

Recombinant Human C-JUN amino acids 1-81 produced in E.coli is a non-glycosylated, polypeptide chain having a molecular mass of 52kD. Recombinant C-JUN is a maltose binding protein (MBP) fusion protein with an amino-terminal polyhistidine tag and purified by proprietary chromatographic techniques.\n\nBiological Activity: \nRecombinant human c-Jun is phosphorylatable in vitro, using either recombinant active JNK1 or JNK2, or with JNK immunoprecipitated from stimulated cells. This phosphorylation can be monitored by Western blot analysis using an antibody directed to c-Jun [pS73], in conjunction with chemiluminescence detection methods. Optimization of the cell stimulation protocol, cell lysis procedure, and reaction conditions may be required for each specific application. Please note: Kinase activity may vary depending on the substrate and reaction conditions.\n\nStorage: \nStore at 4 degrees C if entire vial will be used within 1-2 weeks. Store, frozen at -20 degrees C for longer periods of time. Please avoid freeze-thaw cycles.

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SPECIFICATIONS

Catalog Number

C5815-02

Size

2ug

Form

Supplied as a lyophilized powder without additives.

Purity

(same/more than) 95% (SDS-PAGE)

References

1. ErbB4 (JM-b/CYT-1)-induced expression and phosphorylation of c-Jun is abrogated by human papillomavirus type 16 E5 protein.\n\nOncogene 2006 Jul 3;\n\n2. Constitutive ALK5-Independent c-Jun N-Terminal Kinase Activation Contributes to Endothelin-1 Overexpression in Pulmonary Fibrosis: Evidence of an Autocrine Endothelin Loop Operating through the Endothelin A and B Receptors.\n\nMol Cell Biol 2006 Jul;26(14):5518-27\n\n3. Loss of hepatic NF-{kappa}B activity enhances chemical hepatocarcinogenesis through sustained c-Jun N-terminal kinase 1 activation.\n\nProc Natl Acad Sci U S A 2006 Jun 28;\n\n4. Aldose Reductase-Deficient Mice Are Protected From Delayed Motor Ner ve Conduction Velocity, Increased c-Jun NH2-Terminal Kinase Activation, Depletion of Reduced Glutathione, Increased Superoxide Accumulation, and DNA Damage.\n\nDiabetes 2006 Jul;55(7):1946-53\n\n5. Homophilic interactions of the tetraspanin CD151 up-regulate motility and MMP-9 expression of human melanoma cells through adhesion-dependent c-jun activation signaling pathways.\n\nJ Biol Chem 2006 Jun 23;\n\n6. Paclitaxel Enhances Thrombin-Induced Endothelial Tissue Factor Expression via c-Jun Terminal NH2 Kinase Activation.\n\nCirc Res 2006 Jun 22;