Product Name: ERK2 (198-205) pT202
Product Number: PE-04AWC00
Size: 200 µg      Price:32.00
1 mg      $US63.00
Peptide Name: ERK2 (198-205) pT202

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 between subdomains VII and VIII. T202 phosphorylation stimulates phosphotransferase activity.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: GFL-pT-EYV

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys

Peptide Modifications Other: Phosphorylated

Peptide Purity Percent after Synthesis and Purification: ~80

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Storage Stability: solution tends to dimerize

Scientific Background: ERK2 (MAPK1) is a protein-serine/threonine kinase of the CMGC group and MAPK family. It is involved in the MAP Kinase signalling pathway. The MAP kinase pathway can mediate cell adhesion, growth, survival, differentiation, meiosis, mitosis, and other post-mitotic functions. Phosphorylation of T185 and Y187 by MEK1 an MEK2 increases its phosphotransferase activity. It phosphorylates many diffrent transcription factors, such as ELK1. It acts as transcriptional repressor by binding directly to DNA. It is essential for cyclin D1 induction. MAPK1 phosphorylates BCL2, which contributes to cell survival, the suppression of the apoptotic effect of BAD and up-regulation of the antiapoptotic protein MCL-1. It regulates accumulation of p53 during DNA damage response. ERK2 appears to be a tumour requiring protein (TRP). The active form of the protein kinase normally acts to promote tumour cell proliferation. ERK2 has been linked with the Ewing's Family of tumours, which are rare cancers that are similar to medullablastoma and cerebral primitive neuroectodermal tumours. It is constitutively active in many human tumours, primarily due to altered Ras, Raf, EGFR or other upstream oncoproteins.