Product Name: MST1 (172-190) pT175+pT177+pT183+pT187
Product Number: PE-04AWO70
Size: | 200 µg | | Price: | 99.00 |
| 1 mg | | $US | 198.00 |
Peptide Name: MST1 (172-190) pT175+pT177+pT183+pT187
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. T183 phosphorylation stimulates phosphotransferase activity. T175 and T177 phosphorylation are predicted to stimulate phosphotransferase activity. T187 is a putative phosphorylation site that is predicted to be inhibitory.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: GQL-pT-D-pT-MAKRN-pT-VIG-pT-PFW
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: βAla-Cys
Peptide Modifications Other: Phosphorylated
Peptide Molecular Mass Calculated: 2671.6 Da
Peptide Purity Percent after Synthesis and Purification: ~80
Peptide Appearance: White powder
Peptide Form: Solid
Storage Conditions: -20°C
Storage Stability: n.d.
Scientific Background: MST1 (STK4) is a protein-serine/threonine kinase of the STE group and STE20 family. It can induce apoptosis following stress activation. MST1 activity can occur in the nucleus and can be via condensation of chromatin and fragmentation of intranucleosomal DNA. It is activated by caspase-cleavage. Full activation requires homodimerization and autophosphorylation of T183; MST1 phosphotransferase activity can be lost with a T183A mutation. Proteolytic cleavage of MST1 during apoptosis can be reduced with the D326N and D349N mutations. Homodimerization and autophosphorylation are lost with a L444P mutation. It leads to the inactivation of the YAP1 oncoprotein by activating downstream kinases such as LATS1 and LATS2, which phosphorylate YAP1 to prevent it from translocating to the nucleus and transcribing cell proliferation and migration genes. MST1 can also promote apoptosis by preventing the deacetylation of p53/TP53, thus promoting p53-dependent transcription and apoptosis. It is also able to inhibit the PKB/Akt1 pathway. MST1 is linked to pancreatic cancer, which is a rare cancer that does not have characteristic symptoms but is related to the integrated breast cancer and pancreatic cancer pathways.