c-Jun ELISA Kit (DEIA-XYA909)

Regulatory status: For research use only, not for use in diagnostic procedures.

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nuclear, cell lysates
Species Reactivity
Human, Mouse, Rat
Contents of Kit
1. 12x 8-Well dsDNA Oligonucleotide Coated Microstrips
2. 100x Anti-Phospho Target Primary Antibody
3. 100x Anti-Target Primary Antibody
4. HRP-Conjugated Anti-Rabbit IgG Secondary Antibody
5. Nuclear Lysate Positive Control
6. Wild-Type Consensus dsDNA Oligonucleotide
7. Mutant Consensus dsDNA Oligonucleotide
8. 10x Wash Buffer
9. 2x Binding Buffer
10. Primary Antibody Diluent
11. 100x Protease and Phosphatase Inhibitors
12. Nuclear Wash Buffer
13. Cytoplasmic Extraction Buffer
14. Nuclear Extraction Buffer
15. Ready-to-Use Substrate
16. Stop Solution
17. Adhesive Plate Seals
18. Technical Manual
4°C/6 Months


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miR-128 regulated the proliferation and autophagy in porcine adipose-derived stem cells through targeting the JNK signaling pathway


Authors: Gao, Pengfei; Wang, Haizhen; Liu, Juan; Wu, Yiqi; Hei, Wei; He, Zhiqiang; Cai, Chunbo; Guo, Xiaohong; Cao, Guoqing; Li, Bugao

Purpose microRNA-128 (miR-128), a brain-enriched microRNA, has been reported to play a crucial role in the treatment of diseases. The c-Jun N-terminal kinase (JNK) signaling pathway exerts various biological functions such as regulation of cell proliferation, differentiation and apoptosis. In this study, we investigated the role of the miRNA-128-JNK signaling pathway in proliferation, apoptosis and autophagy of porcine adipose-derived stem cells (ASCs). Methods After over-expressing miR-128 in porcine ASCs, cell proliferation was determined by 2,3-Bis-(2-Methoxy-4-Nitro-5-Sulfophenyl)-2H-Tetrazolium-5-Carboxanilide (XTT) method, cell apoptosis was observed by Flow cytometry (FCM), the expression of miR-128, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) was measured by RNA preparation and reverse transcription polymerase chain reaction (RT-PCR), and protein expression of JNK, phosphorylated JNK (p-JNK) and LC3B was analyzed by Western Blot analysis. Results The over-expression of miR-128 potently promoted cell proliferation and autophagy while suppressed the apoptosis of porcine ASCs. In addition, the down-regulated expression level of p-JNK was detected in miR-128-over-expressed porcine ASCs. However, followed by the block of the JNK signaling pathway using SP600125 inhibitor, the effects of miR-128 on the proliferation, apoptosis and autophagy of porcine ASCs were significantly suppressed. Conclusion It is demonstrated that the miR-128-JNK signaling pathway is a potential therapeutic target for the treatment of obesity.

Effects of a Risk-Stratified Treatment in Patients with Chronic Back Pain in Rehabilitation: Results of a Controlled Clinical Trial (Jun, 10.1055/a-1205-1380, 2020)


Authors: Schmidt, Christian; Bernert, Sebastian; Sing, Matthias; Fahrenkrog, Sandra; Urbanski-Rini, Dominika; Gottfried, Thomas; Spyra, Karla

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