Product Pathways - MAPK Signaling
JNK1 (2C6) Mouse mAb #3708
|3708S||100 µl (10 western blots)||---||In Stock||---|
|3708||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Monkey||Endogenous||46, 54||Mouse IgG1|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Specificity / Sensitivity
JNK1 (2C6) Mouse mAb detects endogenous levels of total JNK1 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a recombinant protein corresponding to the amino terminus of human JNK1.
Western blot analysis of HeLa cell extracts, untransfected (lane 1), mock-transfected (lane 2) or transfected with SignalSilence® SAPK/JNK siRNA I #6232 (lane 3) or SignalSilence® SAPK/JNK siRNA II #6233 (lane 4) for 72 hours, using JNK1 (2C6) Mouse mAb.
The stress-activated protein kinase/Jun-amino-terminal kinase SAPK/JNK is potently and preferentially activated by a variety of environmental stresses including UV and gamma radiation, ceramides, inflammatory cytokines, and in some instances, growth factors and GPCR agonists (1-6). As with the other MAPKs, the core signaling unit is composed of a MAPKKK, typically MEKK1-MEKK4, or by one of the mixed lineage kinases (MLKs), which phosphorylate and activate MKK4/7. Upon activation, MKKs phosphorylate and activate the SAPK/JNK kinase (2). Stress signals are delivered to this cascade by small GTPases of the Rho family (Rac, Rho, cdc42) (3). Both Rac1 and cdc42 mediate the stimulation of MEKKs and MLKs (3). Alternatively, MKK4/7 can be activated in a GTPase-independent mechanism via stimulation of a germinal center kinase (GCK) family member (4). There are three SAPK/JNK genes each of which undergoes alternative splicing, resulting in numerous isoforms (3). SAPK/JNK, when active as a dimer, can translocate to the nucleus and regulate transcription through its effects on c-Jun, ATF-2, and other transcription factors (3,5).
- Davis, R.J. (1999) Biochem Soc Symp 64, 1-12.
- Ichijo, H. (1999) Oncogene 18, 6087-93.
- Kyriakis, J.M. and Avruch, J. (2001) Physiol Rev 81, 807-69.
- Kyriakis, J.M. (1999) J Biol Chem 274, 5259-62.
- Leppä, S. and Bohmann, D. (1999) Oncogene 18, 6158-62.
- Whitmarsh, A.J. and Davis, R.J. (1998) Trends Biochem Sci 23, 481-5.
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