|Tested species reactivity||Human, Mouse, Rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||A synthetic phosphopeptide derived from human COT around the phosphorylation site of Thr290 (R-G-TP-E-I)|
|Purification||Antigen affinity chromatography|
|Storage buffer||Dulbecco's PBS, pH 7.4, with 50% glycerol, 150mM NaCl|
|Contains||0.02% sodium azide|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:50-1:100|
|Western Blot (WB)||1:500-1:1000|
* 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.
The role of mitogen-activated protein kinases (MAPKs) in cell signaling pathways is well established. The rat gene Tpl-2, for tumor progression locus 2, and the human and mouse homologues c-Cot, for cancer osaka thyroid oncogene, encode a proto-oncogene serine/threonine protein kinase that was shown to play a role in the functional activation of the MAP kinase pathway. Overexpression of Cot induces MAP kinase activation in COS-1 and NIH/3T3 cells. Cot-mediated activation of MAP kinase is inhibited by both Ras N17, a dominant negative mutant of c-H-Ras, and Raf-1s621A, a dominant negative mutant of Raf-1, suggesting that Cot functions upstream of Ras and Raf-1.Other studies have shown that a kinase-negative, dominant negative mutant of Cot partially blocks Ras or Raf-1-induced MAP kinase activation, arguing that Cot functions downstream of Ras and Raf-1.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.