Western blot analysis of Phospho-TAK1 pThr184/187 in extracts from 293 IL-1R cells, untreated or treated for 10 minutes with IL-1, using Phospho-TAK1 pThr184/187 monoclonal antibody (Product # MA5-15073) (upper) or a TAK1 polyclonal antibody (lower).
|Tested species reactivity||Bovine, Chicken, Human, Mouse, Rat, Xenopus, Zebrafish|
|Published species reactivity||Not Applicable|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Phosphopeptide corresponding to residues surrounding pThr184 and pThr187 of human TAK1|
|Storage buffer||0.01M HEPES, pH 7.5, with 0.15M NaCl, 100µg/ml BSA, 50% glycerol|
|Contains||<0.02% sodium azide|
|Tested Applications||Dilution *|
|Western Blot (WB)||1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Flow Cytometry (Flow)||See 1 publications below|
It is not recommended to aliquot this antibody.
The protein encoded by this gene is a member of the serine/threonine protein kinase family. This kinase mediates the signaling transduction induced by TGF beta and morphogenetic protein (BMP), and controls a variety of cell functions including transcription regulation and apoptosis. In response to IL-1, this protein forms a kinase complex including TRAF6, MAP3K7P1/TAB1 and MAP3K7P2/TAB2; this complex is required for the activation of nuclear factor kappa B. This kinase can also activate MAPK8/JNK, MAP2K4/NhpK4, and thus plays a role in the cell response to environmental stresses. Four alternatively spliced transcript variants encoding distinct isoforms have been reported.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
TAK1 modulates satellite stem cell homeostasis and skeletal muscle repair.
MA5-15073 was used in flow cytometry to characterize TAK1 and modulation of skeletal muscle repair and satelline stem cell homeostasis
|Ogura Y,Hindi SM,Sato S,Xiong G,Akira S,Kumar A||Nature communications (6:null)||2015|