Product Name: p38a (179-185) pT180+pY182
Product Number: PE-04ADE99
Size: 200 µg      Price:66.00
1 mg      $US132.00
Peptide Name: p38a (179-185) pT180+pY182

Product Use: Services as a blocking peptide for use with the p38a-pT180+Y182 rabbit polyclonal antibody (Cat. No.: AB-PK740) that is also available from Kinexus. This phosphopeptide may also 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. T180 and Y182 phosphorylation is stimulatory for phosphotransferase activity.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: M-pT-G-pY-VAT

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys
Peptide Modifications Other: Phosphorylated

Peptide Molecular Mass Calculated: 1076.01 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Related Product 1: p38a - pT180+pY182 phosphosite-specific antibody (Cat. No.: AB-PK740)

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.