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BD Phosflow™ PE Mouse anti-JNK (pT183/pY185)
Clone N9-66 (RUO)
Regulatory Status Legend
Any use of products other than the permitted use without the express written authorization of Becton, Dickinson and Company is strictly prohibited.
Preparation And Storage
Product Notices
- This reagent has been pre-diluted for use at the recommended Volume per Test. We typically use 1 × 10^6 cells in a 100-µl experimental sample (a test).
- For fluorochrome spectra and suitable instrument settings, please refer to our Multicolor Flow Cytometry web page at www.bdbiosciences.com/colors.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
- Source of all serum proteins is from USDA inspected abattoirs located in the United States.
Companion Products
The N9-66 monoclonal antibody specifically binds to JNK1 and JNK2 phosphorylated at the pT183/pY185 sites. c-Jun NH2-terminal Kinases (JNKs), also called Stress Activated Protein Kinases (SAPKs), are mitogen-activated protein kinases (MAPKs) with observed molecular weights of ~46 kDa (JNK1) and ~54 kDa (JNK2). Along with the p38 and ERK families, JNK represents one of three major classes of MAPKs. Complete activation of JNK requires the phosphorylation of both Thr183 and Tyr185 that are located in a Thr-X-Tyr motif. Phosphorylation of these residues is carried out by MKK4 and MKK7 that are phosphorylated and activated by MEKKs and MLKs in response to stress signals delivered through small GTPases of the Rho family. Once activated, JNK can translocate into the nucleus and regulate the expression of genes through phosphorylation of c-Jun, ATF-2, and other transcription factors. JNK plays a role in signal transduction in response to cytokines and various forms of environmental stress, such as endotoxins, UV irradiation, heat, and hyperosmolarity. JNK is critical to the regulation of cell growth, apoptosis, and the cellular response to stress, making it an important factor in tumorigenesis and adaptive immunity. During antibody development, the N9-66 monoclonal antibody was found to detect phosphorylated JNK1/2 by Western blot analysis of cellular lysates and by immunofluorescent staining and flow cytometric analysis of fixed and permeabilized cells. This antibody crossreacts with phosphorylated JNK1/2 expressed by mouse cells, as tested by Western blot analysis and flow cytometry.
Development References (4)
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Fleming Y, Armstrong CG, Morrice N, Paterson A, Goedert M, Cohen P. Synergistic activation of stress-activated protein kinase 1/c-Jun N-terminal kinase (SAPK1/JNK) isoforms by mitogen-activated protein kinase kinase 4 (MKK4) and MKK7. Biochem J. 2000; 352:145-154. (Biology). View Reference
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Huang G, Shi LZ, Chi H. Regulation of JNK and p38 MAPK in the immune system: signal integration, propagation and termination. Cytokine. 2009; 48(3):161-169. (Biology). View Reference
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Kyriakis JM, Avruch J. Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammation. Physiol Rev. 2001; 81(2):807-869. (Biology). View Reference
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Wagner EF, Nebreda AR. Signal integration by JNK and p38 MAPK pathways in cancer development. Nat Rev Cancer. 2009; 9(8):537-549. (Biology). View Reference
Please refer to Support Documents for Quality Certificates
Global - Refer to manufacturer's instructions for use and related User Manuals and Technical data sheets before using this products as described
Comparisons, where applicable, are made against older BD Technology, manual methods or are general performance claims. Comparisons are not made against non-BD technologies, unless otherwise noted.
For Research Use Only. Not for use in diagnostic or therapeutic procedures.