Cell Signaling Technology

Product Pathways - MAPK Signaling

JNK2 Antibody #4672

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Hm Mk Endogenous 54 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Hm=Hamster  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

JNK2 Antibody detects endogenous levels of JNK2. It will only recognize the JNK2 Alpha 2 and JNK2 Beta 2 isoforms. It will not recognize JNK2 Alpha 1 and JNK2 Beta 1 isoforms. This antibody does not recognize p38 MAP kinase, p44/42MAP kinase or JNK1.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human JNK2. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293, C2C12, NIH/3T3, PC12, and COS cells, using JNK2 Antibody.

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).

  1. Davis, R.J. (1999) Biochem Soc Symp 64, 1-12.
  2. Ichijo, H. (1999) Oncogene 18, 6087-93.
  3. Kyriakis, J.M. and Avruch, J. (2001) Physiol Rev 81, 807-69.
  4. Kyriakis, J.M. (1999) J Biol Chem 274, 5259-62.
  5. Leppä, S. and Bohmann, D. (1999) Oncogene 18, 6158-62.
  6. Whitmarsh, A.J. and Davis, R.J. (1998) Trends Biochem Sci 23, 481-5.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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