Molecular Formula | C229H345N69O41 |
Molar Mass | 4720.6273 |
Storage Condition | 2-8°C,干燥,密封 |
In vitro study | PR-39, shown to selectively affect proteasomemediated protein degradation in vivo, alters the shape of the 20S and 26S cylinder and affects the binding of 19S caps in a reversible manner. PR-39 specifically blocks degradation of IκBα and HIF-1α by the proteasome. PR-39 (100 nM) blocks TNF-α-induced (1 ng/mL; for 20 minutes) activation of VCAM-1 (2 hours) and ICAM-1 (8 hours) expression in human umbilical vein endothelial cells (HUVEC). PR-39 (10 μM) does not affect the ability to proliferate of ECV304 cell. PR39 is able to inhibit IκBα degradation without significantly affecting overall protein degradation in cells. |
In vivo study | PR-39 (10 mg/kg, intravenously; 1 hour before Caerulein of 50μg/kg, ip) blocks IκBα degradation and NF-κB-dependent transcription in the mouse pancreas after induction of acute pancreatitis. PR-39 (1 μg/kg/day; 7-day intraperitoneal infusion) demonstrates significantly small infarct in C57BL/6 mice. |
biological activity | PR-39 is a kind of natural antibacterial peptide rich in proline and arginine, reversible and allosteric proteasome inhibitors. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of the NF-κB inhibitor IκBα through the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis in mice, suppresses inflammatory responses and significantly reduces myocardial infarct size. |