Cell Signaling Technology

Product Pathways - MAPK Signaling

Phospho-JunB (Thr102/Thr104) (D3C6) Rabbit mAb #8053

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H (M) (R) Endogenous 43 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
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-JunB (Thr102/Thr104) (D3C6) Rabbit mAb recognizes endogenous levels of JunB protein when phosphorylated at Thr102 and/or Thr104. The antibody does not detect non-phosphorylated JunB protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with synthetic phosphopeptides corresponding to residues surrounding Thr102 and Thr104 of human JunB protein.

Western blot analysis of extracts from 293T cells treated with Anisomycin (25 ug/ml) for the time indicated, with or without pretreatment with JNK inhibitor SP600125 (40 min, 50 uM), using Phospho-JunB (Thr102/Thr104) (D3C6) Rabbit mAb (upper) or JunB (C37F9) Rabbit mAb #3753 (lower).

Background

JunB is a basic region, leucine zipper (bZIP) transcription factor belonging to the Jun family that includes c-Jun and JunD. Jun family members homodimerize or heterodimerize with Fos and ATF proteins to form a functional transcription factor AP-1 (activator protein 1), whose activity is regulated by a variety of physiological and pathological stimuli such as growth factors, infections, and stress signals (1-4). While JunB sometimes antagonizes c-Jun transcriptional activity, it may functionally substitute for c-Jun during development in mice (5-7). JunB regulates hematopoietic stem cell number and plays an important role in the pathogenesis of chronic myelogenous leukemia (CML) and acute myeloid leukemia (AML) (8,9).

JunB expression is selectively induced in T helper 2 (Th2) cells during T cell differentiation. JunB interacts with c-Maf, and the resulting complex functions synergistically to activate transcription of Interleukin-4 (IL-4), one of the signature cytokines secreted by Th2 cells. Transcriptional regulation of IL-4 was shown to be enhanced by JNK-mediated phosphorylation of JunB at Thr102 and Thr104 (10). Phosphorylation of these residues enhances DNA binding of the JunB/c-Maf complex at the P1 regulatory site of the IL-4 promoter, leading to Th2-restricted IL-4 expression.

  1. Busch, S.J. and Sassone-Corsi, P. (1990) Trends Genet. 6, 36-40.
  2. Shaulian, E. and Karin, M. (2002) Nat. Cell Biol. 4, E131-E136.
  3. Hess, J. et al. (2004) J. Cell Sci. 117, 5965-5973.
  4. Mechta-Grigoriou, F. et al. (2001) Oncogene 20, 2378-2389.
  5. Chiu, R. et al. (1989) Cell 59, 979-986.
  6. Schütte, J. et al. (1989) Cell 59, 987-997.
  7. Passegué, E. et al. (2002) Nat. Genet. 30, 158-166.
  8. Steidl, U. et al. (2006) Nat. Genet. 38, 1269-1277.
  9. Passegué, E. et al. (2004) Cell 119, 431-443.
  10. Li, B. et al. (1999) EMBO J 18, 420-32.

Application References

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

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