ERK2 (Thr-188)[conserved site], phospho-specific polyclonal, anti-human, mouse, rat, chicken, fish

Background:
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.

Immunogen: Phospho-ERK2 (Thr-188) synthetic peptide (coupled to carrier protein) corresponds to amino acids surrounding Thr-188 in mouse ERK2. This sequence is conserved in human, rat, chicken, and fish ERK2, and is highly conserved in ERK1 (Thr-207), ERK5 (Thr-224), and ERK7 (Thr-180).

Specificity: The antibody detects 42 and 44 kDa* proteins corresponding to ERK1 and ERK2 on SDS-PAGE immunoblots of human A431 epithelial cells stimulated with calyculin A. It does not detect these ERK proteins in control cells or in blots treated with lambda phosphatase.

Buffer/Storage:
Rabbit polyclonal, affinity-purified antibody is supplied in 100µl phosphate-buffered saline, 50% glycerol, 1 mg/ml BSA, and 0.05% sodium azide. Store at –20°C. Stable for 1 year.