Bioactivity | N-Acetyl-Ser-Asp-Lys-Pro (TFA), an endogenous tetrapeptide secreted by bone marrow, is a specific substrate for the N-terminal site of ACE. | ||||||
Invitro | N-Acetyl-Ser-Asp-Lys-Pro is degraded specifically by ACE, and its plasma level rises substantially during ACE inhibitor therapy. Flow cytometry of rat cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro shows significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle. Moreover, phosphorylation and nuclear translocation of Smad2 is decreased in cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro[1]. N-acetyl-seryl-aspartyl-lysyl-proline appears to exert this function by blocking the action of a stem cell-specific proliferation stimulator and acts selectively on quiescent progenitors[2]. N-Acetyl-Ser-Asp-Lys-Pro inhibits collagenase expression and activation is associated with increased expression of TIMP-1 and TIMP-2. N-Acetyl-Ser-Asp-Lys-Pro normalizes the IL-1β-mediated increase in MMP-2 and MMP-9 activities and MMP-13 expression[3]. | ||||||
Name | N-Acetyl-Ser-Asp-Lys-Pro TFA | ||||||
Sequence | Ac-Ser-Asp-Lys-Pro | ||||||
Shortening | Ac-SDKP | ||||||
Formula | C22H34F3N5O11 | ||||||
Molar Mass | 601.53 | ||||||
Transport | Room temperature in continental US; may vary elsewhere. | ||||||
Storage | Sealed storage, away from moisture
*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture) |