|Application ||WB, IHC-P, E|
|Other Accession||Q9ESS0, Q0IID7|
|Calculated MW||52642 Da|
|Antigen Region||1-30 aa|
|Other Names||Dual specificity protein phosphatase 10, Mitogen-activated protein kinase phosphatase 5, MAP kinase phosphatase 5, MKP-5, DUSP10, MKP5|
|Target/Specificity||This DUSP10 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human DUSP10.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||DUSP10 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Protein phosphatase involved in the inactivation of MAP kinases. Has a specificity for the MAPK11/MAPK12/MAPK13/MAPK14 subfamily. It preferably dephosphorylates p38.|
|Cellular Location||Cytoplasm. Nucleus.|
|Tissue Location||Detected in brain.|
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Provided below are standard protocols that you may find useful for product applications.
Dual specificity protein phosphatases inactivate their target kinases by dephosphorylating both the phosphoserine/threonine and phosphotyrosine residues. They negatively regulate members of the MAPK superfamily (MAPK/ERK, SAPK/JNK, p38), which is associated with cellular proliferation and differentiation. Different members of this family of dual specificity phosphatases show distinct substrate specificities for MAPKs, different tissue distribution and subcellular localization, and different modes of inducibility of their expression by extracellular stimuli. DUSP10 binds to and inactivates p38 and SAPK/JNK, but not MAPK/ERK. Its subcellular localization is unique; it is evenly distributed in both the cytoplasm and the nucleus. The protein is widely expressed in various tissues and organs, and its expression is elevated by stress stimuli.
Tanoue, T., et al., J. Biol. Chem. 274(28):19949-19956 (1999).
Theodosiou, A., et al., Oncogene 18(50):6981-6988 (1999).
Martell, K.J., et al., Mol. Cells 8(1):2-11 (1998).
Masuda, K., et al., Cytogenet. Cell Genet. 90 (1-2), 71-74 (2000) (): ().
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