Kobayashi K, Smith J A
J Biol Chem. 1987 Aug 25;262(24):11435-45.
Acyl-peptide hydrolase, which catalyzes the hydrolysis of an N-terminally acetylated peptide to release an N-acetylamino acid, was isolated from rat liver and found to be N-terminally blocked. The kinetics of the hydrolysis of acetyl (Ac)-Ala-Ala, Ac-Ala-Ala-Ala, acetylalanine p-nitroanilide, and acetylalanine beta-naphthylamide were investigated. The Km values were between 1 and 9 mM, and the Vmax values were between 100 and 500 nmol/min/micrograms of enzyme. The enzyme activity toward acetylalanine p-nitroanilide and acetylalanine beta-naphthylamide was activated by the presence of Cl- and SCN- at concentrations between 0.1 and 0.5 M. By contrast, the activity toward Ac-Ala-Ala and Ac-Ala-Ala-Ala was inhibited by these anions. Among a series of divalent cations, Zn2+ was demonstrated to be the most potent inhibitor. The enzyme was inactivated by the addition of diisopropyl fluorophosphate, diethyl pyrocarbonate. Woodward's Reagent K, and glycine methyl ester/carbodiimide. Titration by diisopropyl fluorophosphate showed 0.7 mol of active serine/mol of enzyme subunit, which was confirmed by the incorporation of [3H]diisopropyl fluorophosphate into the enzyme. Acetylalanine chloromethyl ketone inactivated the enzyme following pseudo-first order kinetics; and Ac-Ala, a competitive inhibitor, protected the enzyme from this inactivation. Acyl-peptide hydrolase appears to be a serine protease utilizing a charge relay system involving serine, histidine, and, probably, a carboxyl group(s). Two series of acetyl dipeptides, acetylamino acid p-nitroanilides and acetylamino acid beta-naphthylamides, were prepared in order to determine enzyme specificity. The enzyme preferentially removed Ac-Ala, Ac-Met, and Ac-Ser, the most common acetylated N-terminal residues (Persson, B., Flinta, C., von Heijne, G., and Jörnvall, H. (1985) Eur. J. Biochem. 152, 523-527). The enzyme was shown to be useful for deblocking peptides (e.g. alpha-melanocyte-stimulating hormone and acetyl-renin substrate), and the crude enzyme/substrate mixtures were amenable to direct protein sequence analysis.
酰基肽水解酶可催化N - 末端乙酰化肽的水解,释放出N - 乙酰氨基酸,该酶从大鼠肝脏中分离得到,发现其N - 末端被封闭。研究了乙酰(Ac)-丙氨酸 - 丙氨酸、Ac - 丙氨酸 - 丙氨酸 - 丙氨酸、乙酰丙氨酸对硝基苯胺和乙酰丙氨酸β - 萘酰胺的水解动力学。Km值在1至9 mM之间,Vmax值在100至500 nmol/分钟/微克酶之间。氯离子和硫氰酸根离子浓度在0.1至0.5 M之间时,该酶对乙酰丙氨酸对硝基苯胺和乙酰丙氨酸β - 萘酰胺的活性被激活。相比之下,这些阴离子会抑制该酶对Ac - 丙氨酸 - 丙氨酸和Ac - 丙氨酸 - 丙氨酸 - 丙氨酸的活性。在一系列二价阳离子中,Zn2 +被证明是最有效的抑制剂。通过添加二异丙基氟磷酸酯、焦碳酸二乙酯、伍德沃德试剂K和甘氨酸甲酯/碳二亚胺可使该酶失活。用二异丙基氟磷酸酯滴定显示,每摩尔酶亚基有0.7摩尔活性丝氨酸,这通过将[3H]二异丙基氟磷酸酯掺入该酶中得到证实。乙酰丙氨酸氯甲基酮按照假一级动力学使该酶失活;竞争性抑制剂Ac - 丙氨酸可保护该酶不被这种失活作用影响。酰基肽水解酶似乎是一种利用涉及丝氨酸、组氨酸以及可能的羧基的电荷中继系统的丝氨酸蛋白酶。制备了两个系列的乙酰二肽、乙酰氨基酸对硝基苯胺和乙酰氨基酸β - 萘酰胺,以确定酶的特异性。该酶优先去除Ac - 丙氨酸、Ac - 甲硫氨酸和Ac - 丝氨酸,这些是最常见的乙酰化N - 末端残基(佩尔松,B.,弗林塔,C.,冯·海涅,G.,和约恩瓦尔,H.(1985年)《欧洲生物化学杂志》152卷,523 - 527页)。已证明该酶可用于去除肽的封闭基团(例如α - 黑素细胞刺激素和乙酰肾素底物),并且粗酶/底物混合物适用于直接蛋白质序列分析。