Barelli H, Vincent J P, Checler F
Institut de Pharmacologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique, Université Nice Sophia Antipolis, Valbonne, France.
Eur J Biochem. 1993 Jan 15;211(1-2):79-90. doi: 10.1111/j.1432-1033.1993.tb19872.x.
Endopeptidase 24.16 was purified from rat kidney homogenate on the basis of its ability to generate the biologically inactive degradation products neurotensin (1-10) and neurotensin (11-13). On SDS gels of the proteins pooled after the last purification step, the enzyme appeared homogeneous and behaved as a 70-kDa monomer. The peptidase was not sensitive to specific inhibitors of aminopeptidases, pyroglutamyl aminopeptidase I, endopeptidase 24.11, endopeptidase 24.15, proline endopeptidase and angiotensin-converting enzyme but was potently inhibited by several metal chelators such as o-phenanthroline and EDTA and was blocked by divalent cations. The specificity of endopeptidase 24.16 towards peptides of the tachykinin, opioid and neurotensin families was examined by competition experiments of tritiated neurotensin hydrolysis as well as HPLC analysis. These results indicated that endopeptidase 24.16 could discriminate between peptides belonging to the same family. Neurotensin, Lys8-Asn9-neurotensin(8-13) and xenopsin were efficiently hydrolysed while neuromedin N and kinetensin underwent little if any proteolysis by the peptidase. Analogously, substance P and dynorphins (1-7) and (1-8) were readily proteolysed by endopeptidase 24.16 while neurokinin A, amphibian tachykinins and leucine or methionine enkephalins totally resisted degradation. By Triton X-114 phase separation, 15-20% of endopeptidase 24.16 partitioned in the detergent phase, indicating that renal endopeptidase 24.16 might exist in a genuine membrane-bound form. The equipotent solubilization of the enzyme by seven detergents of various critical miscellar concentrations confirmed the occurrence of a membrane-bound counterpart of endopeptidase 24.16. Furthermore, the absence of release elicited by phosphatidylinositol-specific phospholipase C suggested that the enzyme was not attached by a glycosyl-phosphatidylinositol anchor in the membrane of renal microvilli. Finally, endopeptidase 24.16 could not be released from these membranes upon trypsinolysis.
基于内肽酶24.16能够产生无生物活性的降解产物神经降压素(1 - 10)和神经降压素(11 - 13)的能力,从大鼠肾脏匀浆中纯化出了该酶。在最后一步纯化步骤后合并的蛋白质的SDS凝胶上,该酶呈现均一性,表现为70 kDa的单体。该肽酶对氨肽酶、焦谷氨酰氨肽酶I、内肽酶24.11、内肽酶24.15、脯氨酸内肽酶和血管紧张素转换酶的特异性抑制剂不敏感,但被几种金属螯合剂如邻菲罗啉和EDTA强烈抑制,并被二价阳离子阻断。通过氚标记的神经降压素水解竞争实验以及HPLC分析,研究了内肽酶24.16对速激肽、阿片肽和神经降压素家族肽段的特异性。这些结果表明,内肽酶24.16可以区分属于同一家族的肽段。神经降压素、赖氨酸8 - 天冬酰胺9 - 神经降压素(8 - 13)和异速激肽被有效水解,而神经介素N和激肽原很少或几乎不被该肽酶进行蛋白水解。类似地,P物质、强啡肽(1 - 7)和(1 - 8)很容易被内肽酶24.16蛋白水解,而神经激肽A、两栖类速激肽以及亮氨酸或甲硫氨酸脑啡肽完全抵抗降解。通过Triton X - 114相分离,15% - 20%的内肽酶24.16分配到去污剂相中,表明肾内肽酶24.16可能以真正的膜结合形式存在。七种不同临界胶束浓度的去污剂对该酶的等效增溶作用证实了内肽酶24.16存在膜结合对应物。此外,磷脂酰肌醇特异性磷脂酶C未引发释放,这表明该酶不是通过糖基磷脂酰肌醇锚定在肾微绒毛膜上。最后,胰蛋白酶消化后,内肽酶24.16不能从这些膜上释放出来。