产品
编 号：F600770
分子式：C229H346N70O40
分子量：4719.74
分子式：C229H346N70O40
分子量：4719.74
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CAS No: 139637-11-9
产品详情
生物活性：
PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice.
体内研究：
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.
体外研究：
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.
PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice.
体内研究：
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.
体外研究：
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.
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