Product Name: p38a (179-185) pT182
Product Number: PE-04AWE00
Size: 200 µg      Price:11.00
1 mg      $US21.00
Peptide Name: p38a (179-185) pT182

Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases. T182 phosphorylation stimulates phosphotransferase activity. This phosphosite is located in the kinase activation loop between catalytic subdomains VII and VIII.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: MTG-pY-VAT

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys

Peptide Modifications Other: Phosphorylated

Peptide Molecular Mass Calculated: 995.1 Da

Peptide Purity Percent after Synthesis and Purification: >50

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Storage Stability: solution tends to dimerize

Scientific Background: p38a (MAPK14) is a protein-serine/threonine kinase of the CMGC group and MAPK family, and a member of the p38 stress-activated MAP kinases. It is activated by pro-inflammatory cytokines, environmental stress and LPS. Phosphorylation at T180 and Y182 increases its phosphotransferase activity. These phospho-sites are targeted by MKK3 (MAP2K3), MKK6 (MAP2K6), and potentially also MKK4 (MAP2K4). Phosphorylation at Y323 also increases its phosphotransferase activity. It is inhibited by dual specificity phosphatases, such as DUSP1. Phosphorylation at T123 inhibits phosphotransferase activity and interaction with MKK6 and MAPKAPK2. Its many substrates include the transcription regulators ATF2, MEF2C, and MAX; the cell cycle regulator CDC25B; and p53, which indicates that p38a plays a role in stress-related transcription and in cell cycle regulation, as well as in the genotoxic stress response. It is a key player in the maintenance of hematopoiesis homeostasis, as it balances both proliferative and growth inhibitory signals from growth factors/cytokines that regulate hematopoiesis. Alterations in this controlled balance could result in either overproduction or depletion of myelosuppressive cytokines, which could lead to the development of various types of bone marrow failures. p38a may be also involved in drug resistance development of acute myeloid leukemias.