SignalSilence® SAPK/JNK siRNA I #6232
Supporting Data
| REACTIVITY | H |
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
CST recommends transfection with 100 nM SAPK/JNK siRNA I 48 to 72 prior to cell lysis. For transfection procedure, follow protocol provided by the transfection reagent manufacturer. Please feel free to contact CST with any questions on use.
Each vial contains the equivalent of 100 transfections, which corresponds to a final siRNA concentration of 100 nM per transfection in a 24-well plate with a total volume of 300 μl per well.
Storage
Product Description
Quality Control
Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
Background
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.
限制使用
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