DUSP16/MKP7 (D5F4) Rabbit mAb #5523
- WB
Supporting Data
REACTIVITY | H M R Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 79 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Source / Purification
Background
DUSP16/MKP7 is a negative regulator of the JNK/SAPK family of stress-activated MAP kinases. It inhibits JNK-mediated signaling events by dephosphorylating threonine and tyrosine residues within the activation loop of JNK proteins, effectively preventing further activation of downstream effectors (7,8). DUSP16/MKP7 expression has been shown to be upregulated after oxidative stress, presumably as a means of supressing JNK activity in order to return the cells to a homeostatic state (9). DUSP16 is normally turned over at a high-rate in most cells, but the stability of the protein can be enhanced by Erk1/2-mediated phosphorylation on Ser446, indicating that activation of mitogenic signaling pathways can supress stress-response pathways via stabilization of a JNK phosphatase (10,11). Despite demonstrating a substrate preference towards JNK proteins, DUSP16/MKP7 has been shown to interact with other MAPK family members (Erk1/2, p38 MAPKs) as well as scaffolding proteins that may coordinate its activity and specificity (12,13).
DUSP16 is epigenetically silenced in Burkitt's lymphoma by increased methylation of the 5' regulatory regions of the gene (14). Methylation of the DUSP16 gene and expression of DUSP16 protein inversely correlate with increased basal levels of JNK acitvitiy, suggesting DUSP16/MKP7 may play a critical role in maintaining JNK signaling in an "off" state in normal cells (14). More recently, DUSP16/MKP7 has been shown to play a crucial role in T helper (Th) cell differentiation into Th1 and Th2 cells, mediated by JNK signaling pathways (15). DUSP16/MKP7 expression is preferentially high in Th2 cells and low in Th1 cells during differentiation, resulting in either low (Th2) or high (Th1) JNK activity. This suggests that DUSP16 expression may be a regulator of Th cell balance (15).
- Camps, M. et al. (2000) FASEB J 14, 6-16.
- Theodosiou, A. and Ashworth, A. (2002) Genome Biol 3, REVIEWS3009.
- Salojin, K. and Oravecz, T. (2007) J Leukoc Biol 81, 860-9.
- Tanoue, T. et al. (2002) J Biol Chem 277, 22942-9.
- Dickinson, R.J. and Keyse, S.M. (2006) J Cell Sci 119, 4607-15.
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- Matsuguchi, T. et al. (2001) Mol Cell Biol 21, 6999-7009.
- Masuda, K. et al. (2001) J Biol Chem 276, 39002-11.
- Teng, C.H. et al. (2007) J Biol Chem 282, 28395-407.
- Katagiri, C. et al. (2005) J Biol Chem 280, 14716-22.
- Masuda, K. et al. (2003) J Biol Chem 278, 32448-56.
- Willoughby, E.A. and Collins, M.K. (2005) J Biol Chem 280, 25651-8.
- Willoughby, E.A. et al. (2003) J Biol Chem 278, 10731-6.
- Lee, S. et al. (2010) Br J Cancer 103, 265-74.
- Musikacharoen, T. et al. (2011) J Biol Chem 286, 24896-905.
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