Cell Signaling Technology

Product Pathways - MAPK Signaling

Phospho-c-Jun (Thr91) Antibody #2303

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Endogenous 48 Rabbit

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

Protocols

Specificity / Sensitivity

Phospho-c-Jun (Thr91) Antibody detects endogenous levels of total c-Jun protein only when phosphorylated at threonine 91.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues around Thr91 of human c-Jun. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from untreated or UV-treated COS and NIH/3T3 cells, using Phospho-c-Jun (Thr91) Antibody (upper) or c-Jun (60A8) Rabbit mAb #9165 (lower).

Background

c-Jun is a member of the Jun family containing c-Jun, JunB, and JunD, and is a component of the transcription factor activator protein-1 (AP-1). AP-1 is composed of dimers of Fos, Jun, and ATF family members and binds to and activates transcription at TRE/AP-1 elements (reviewed in 1). Extracellular signals including growth factors, chemokines, and stress activate AP-1-dependent transcription. The transcriptional activity of c-Jun is regulated by phosphorylation at Ser63 and Ser73 through SAPK/JNK (reviewed in 2). Knock-out studies in mice have shown that c-Jun is essential for embryogenesis (3), and subsequent studies have demonstrated roles for c-Jun in various tissues and developmental processes including axon regeneration (4), liver regeneration (5), and T cell development (6). AP-1 regulated genes exert diverse biological functions including cell proliferation, differentiation, and apoptosis, as well as transformation, invasion and metastasis, depending on cell type and context (7-9). Other target genes regulate survival, as well as hypoxia and angiogenesis (8,10). Research studies have implicated c-Jun as a promising therapeutic target for cancer, vascular remodeling, acute inflammation, and rheumatoid arthritis (11,12).

The multisite phosphorylation of the transcription factor c-Jun has been reinvestigated recently (14). The phosphorylation of Thr91 and Thr93 induces a change in the conformation of c-Jun that enhances accessibility of the carboxy-terminal sites to a protein phosphatase(s) (15). The identity of the protein kinase that phosphorylates Thr91 and Thr93 in vivo is unknown.

  1. Jochum, W. et al. (2001) Oncogene 20, 2401-12.
  2. Davis, R.J. (2000) Cell 103, 239-52.
  3. Hilberg, F. et al. (1993) Nature 365, 179-81.
  4. Raivich, G. et al. (2004) Neuron 43, 57-67.
  5. Behrens, A. et al. (2002) EMBO J 21, 1782-90.
  6. Riera-Sans, L. and Behrens, A. (2007) J Immunol 178, 5690-700.
  7. Leppä, S. and Bohmann, D. (1999) Oncogene 18, 6158-62.
  8. Shaulian, E. and Karin, M. (2002) Nat Cell Biol 4, E131-6.
  9. Weiss, C. and Bohmann, D. (2004) Cell Cycle 3, 111-3.
  10. Karamouzis, M.V. et al. (2007) Mol Cancer Res 5, 109-20.
  11. Kim, S. and Iwao, H. (2003) J Pharmacol Sci 91, 177-81.
  12. Dass, C.R. and Choong, P.F. (2008) Pharmazie 63, 411-4.
  13. Morton, S. et al. (2003) EMBO J 22, 3876-86.
  14. Papavassiliou, A.G. et al. (1995) EMBO J 14, 2014-9.

Application References

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

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