Product Name: ERK4 (183-189) pS186
Product Number: PE-04ATR01
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Peptide Name: ERK4 (183-189) pS186
Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain activation T loop region between subdomains VII and VIII. S186 phosphorylation stimulates interaction with MAPKAPK5 and probably phosphorylation stimulates phosphotransferase activity.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: GYL(pS)EGL
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Modifications Other: Phosphorylated
Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain activation T loop region between subdomains VII and VIII. S186 phosphorylation stimulates interaction with MAPKAPK5 and probably phosphorylation stimulates phosphotransferase activity.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: GYL(pS)EGL
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Modifications Other: Phosphorylated
Storage Conditions: -20°C
Scientific Background: ERK4 (MAPK4) is a protein-serine/threonine kinase of the CMGC group and MAPK family. It functions to phosphorylate microtubule-associated protein 2 (MAP2) and MAPKAPK5, which may have a role in promoting the entrance of cells into the cell cycle. ERK3 and ERK4 share high sequence homology and are hypothesized to be paralogues. In animal studies, mice lacking ERK3 show a phenotype that closely resembles human pulmonary immaturity, along with reduced fetal growth potential and significantly lower neonatal survival rates. Additional loss of ERK4 in mice lacking ERK3 does not result in the worsening of symptoms of either the neonatal growth deficiency or the pulmonary immaturity phenotype, indicating that ERK4 is dispensible for mouse embryonic development with regards to pulmonary immaturity and growth potential. Therefore, reduced ERK4 protein expression may contribute to the pathogenesis of pulmonary immaturity, potentially due to a reduced entrance of cells into the cell cycle during pulmonary development.
© Kinexus Bioinformatics Corporation 2017