Background:

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. To explain these contrasting findings, it has been suggested that Cot, Ras and Raf-1 may form a multimeric complex that phosphorylates MEK-1. Cot has also been shown to be implicated in T lymphocyte activation. Two forms of Cot are produced by alternative initiation of translation.

Alternative names:

MAP3K8; COT; ESTF; Mitogen-activated protein kinase kinase kinase 8; Cancer Osaka thyroid oncogene; Proto-oncogene c-Cot; Serine/threonine-protein kinase cot; Tumor progression locus 2; TPL-2

Clonality:

Polyclonal

Reactivity:

Human,Mouse,Rat

Source:

Rabbit

Isotype:

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Immunogen:

Synthesized peptide derived from human Cot around the phosphorylation site of T290.

Concentration:

1mg/ml

Applications:

WB, IHC, IF, ELISA

Recommende dilutions:

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Storage:

PBS with 0.02% sodium azide and 50% glycerol pH 7.4. Store at -20°C. Avoid repeated freeze-thaw cycles.

More info:

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