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139637-11-9

中文名稱 H-ARG-ARG-ARG-PRO-ARG-PRO-PRO-TYR-LEU-PRO-ARG-PRO-ARG-PRO-PRO-PRO-PHE-PHE-PRO-PRO-ARG-LEU-PRO-PRO-ARG-ILE-PRO-PRO-GLY-PHE-PRO-PRO-ARG-PHE-PRO-PRO-ARG-PHE-PRO-NH2
英文名稱 PR 39 (PORCINE)
CAS 139637-11-9
分子式 C229H345N69O41
分子量 4720.63
MOL 文件 139637-11-9.mol
更新日期 2024/12/31 15:15:35
139637-11-9 結(jié)構(gòu)式 139637-11-9 結(jié)構(gòu)式

基本信息

中文別名
抗菌肽PR 39 (PORCINE)
H-ARG-ARG-ARG-PRO-ARG-PRO-PRO-TYR-LEU-PRO-ARG-PRO-ARG-PRO-PRO-PRO-PHE-PHE-PRO-PRO-ARG-LEU-PRO-PRO-ARG-ILE-PRO-PRO-GLY-PHE-PRO-PRO-ARG-PHE-PRO-PRO-ARG-PHE-PRO-NH2
英文別名
PR 39
PR 39 (PORCINE)
PR-39, PORCINE, SYNTHETIC
M.W. 4719.64 C229H346N70O40
L-Prolinamide, L-arginyl-L-arginyl-L-prolyl-L-arginyl-L-prolyl-L-prolyl-L-tyrosyl-L-leucyl-L-prolyl-L-arginyl-L-prolyl-L-arginyl-L-prolyl-L-prolyl-L-prolyl-L-phenylalanyl-L-phenylalanyl-L-prolyl-L-prolyl-L-arginyl-L-leucyl-L-prolyl-L-prolyl-L-arginyl-L-isoleucyl-L-prolyl-L-prolylglycyl-L-phenylalanyl-L-prolyl-L-prolyl-L-arginyl-L-phenylalanyl-L-prolyl-L-prolyl-L-arginyl-L-phenylalanyl-

物理化學(xué)性質(zhì)

儲存條件Desiccate at -20°C
溶解度Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
形態(tài)粉末

常見問題列表

生物活性
PR-39 是富含脯氨酸和精氨酸的天然抗菌肽,是一種非競爭性,可逆和變構(gòu)的蛋白酶體 (proteasome) 抑制劑。PR-39 可逆地結(jié)合到蛋白酶體的 α7 亞基上,并通過泛素-蛋白酶體途徑阻斷 NF-κB 抑制劑 IκBα 的降解。PR-39 刺激小鼠的血管生成,抑制炎癥反應(yīng)并顯著減小心肌梗死面積。
體外研究

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.

體內(nèi)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.

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