Cell Signaling Technology

Product Pathways - MAPK Signaling

SAPK/JNK Antibody #9252

Applications Reactivity MW (kDa) Source
W H M R Hm B Z 46 JNK1. 54 JNK2/3. Rabbit

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

Specificity / Sensitivity

SAPK/JNK Antibody detects endogenous levels of total SAPK/JNK protein.

Source / Purification

Polyclonal antibodies are produced by immunizing rabbits with a GST/human JNK2 fusion protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293 and SK-N-MC cells, untreated or UV-treated (40 J/m2), using Phospho-SAPK/JNK Antibody #9251 (upper) or SAPK/JNK Antibody (lower).

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, by growth factors and GPCR agonists (1-6). As with the other MAPKs, the core signaling unit is composed of a MAPKKK, typically MEKK1-4, or by one of the mixed lineage kinases (MLKs), which phosphorylate and activate MKK4-7, which then 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 by a pathway independent of small GTPases via stimulation of a member of the germinal center kinase (GCK) family (4). There are three SAPK/JNK genes with further diversification resulting from alternative splicing (3). Active SAPK/JNK dimers can translocate to the nucleus to 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, 6087-6093.
  3. Kyriakis, J.M. and Avruch, J. (2001) Physiol. Rev. 81, 807-869.
  4. Kyriakis, J.M. (1999) J. Biol. Chem. 274, 5259-5262.
  5. Leppa, S. and Bohmann, D. (1999) Oncogene 18, 6158-6162.
  6. Whitmarsh, A.J. and Davis, R.J. (1998) Trends Biochem. Sci. 23, 481-485.

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