The ERK1/2 (p44/42) MAPK signaling pathway can be activated in response to a diverse range of extracellular stimuli including mitogens, growth factors, and cytokines. Upon stimulation, a sequential three-part MAP kinase cascade is initiated, consisting of a MAP kinase kinase kinase (MAPKKK), a MAP kinase kinase (MAPKK), and a MAP kinase (MAPK). Activation of the MAPKs, ERK1 and ERK2, leads to phosphorylation of activation loop residues Thr-202/Tyr-204 and Thr-185/Tyr-187, respectively. In addition to dual phosphorylation, ERK1 and 2 are autophosphorylated on Thr-207 or Thr-188, respectively. This phosphorylation is required for nuclear translocation of ERK, and leads to phosphorylation of several nuclear proteins involved in cardiac hypertrophy. Mouse models with mutation of Thr-188 in ERK2 show that this site is critical for ERK-mediated cardiac hypertrophy. Thus, phosphorylation of Thr-188 in ERK2 may be important for controlling the nuclear functions of activated ERK1 and ERK2.
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Owens, D.M. & Keyse, S.M. (2007) Oncogene 26:3203.
Murphy, L.O. & Blenis, J. (2006) Trends Biochem Sci 31:268.
Roux, P.P. & Blenis, J. (2004) Microbiol Mol Biol Rev 68:320.
*For more information, see UniProt Accession P63085
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*All molecular weights (MW) are confirmed by comparison to Bio-Rad Rainbow Markers and to western blot mobilities of known proteins with similar MW.
This kit contains: