Fidai Insiya, Hocharoen Lalintip, Bradford Seth, Wachnowsky Christine, Cowan J A
Evans Laboratory of Chemistry, The Ohio State University, 100 West 18th Avenue, Columbus, OH, 43210, USA.
J Biol Inorg Chem. 2014 Dec;19(8):1327-39. doi: 10.1007/s00775-014-1190-x. Epub 2014 Sep 9.
Catalytic metallopeptides that target the membrane-associated sortase A transpeptidase have been developed and evaluated as irreversible inactivators of SrtA∆N59 (sortase A, lacking the initial membrane-binding domain). The copper-binding GGH tripeptide ATCUN motif was linked to amidated forms of the cell wall sorting signal, LPET and LPETG, as sortase-targeting moieties. The resulting metallopeptides were used to determine half maximal inhibitory concentrations (IC₅₀) and rate constants for time-dependent sortase A inactivation. Michaelis-Menten behavior was observed for the catalytic metallopeptides, and k(cat), K(M) and k(cat)/K(M) parameters were obtained as 0.080 ± 0.002 min⁻¹, 23 ± 2 μM and 0.0035 ± 0.0003 μM⁻¹ min⁻¹, respectively. Concentration-dependent inhibition of SrtA∆N59 by the metallopeptides revealed IC₅₀ values ranging from 570 to 700 µM, while Cu-GGH, which lacked a targeting motif, had no measurable IC₅₀ value (>2,000 µM). Time-dependent inactivation of SrtA revealed a range of catalytic activities, with Cu-GGHGLPETG-NH2 demonstrating the fastest rate of inactivation in the presence of ascorbate and hydrogen peroxide coreactants. The active site of the enzyme comprises residues Cys-184, Arg-197 and His-120. LC-MS/MS analysis of the reaction products demonstrated modification of Cys-184 to cysteine sulfonic acid (+48 amu). Results obtained from a DTNB assay support oxidation of the Cys-184 residue. LC-MS/MS also suggested oxidation of the Arg-197 containing peptide. 2D NMR analysis was performed to assess the possible oxidation of His-120, however, none was observed. These compounds possess the potential for irreversible inactivation of SrtA through oxidative modification of essential residues required for substrate binding.
已开发出靶向膜相关分选酶A转肽酶的催化金属肽,并将其评估为SrtA∆N59(分选酶A,缺乏初始膜结合结构域)的不可逆失活剂。将铜结合的GGH三肽ATCUN基序与细胞壁分选信号LPET和LPETG的酰胺化形式连接,作为分选酶靶向部分。所得金属肽用于确定半数最大抑制浓度(IC₅₀)和时间依赖性分选酶A失活的速率常数。观察到催化金属肽呈现米氏动力学行为,获得的k(cat)、K(M)和k(cat)/K(M)参数分别为0.080±0.002 min⁻¹、23±2 μM和0.0035±0.0003 μM⁻¹ min⁻¹。金属肽对SrtA∆N59的浓度依赖性抑制显示IC₅₀值范围为570至700 μM,而缺乏靶向基序的Cu-GGH没有可测量的IC₅₀值(>2,000 μM)。SrtA的时间依赖性失活显示出一系列催化活性,在抗坏血酸和过氧化氢共反应物存在下,Cu-GGHGLPETG-NH2表现出最快的失活速率。该酶的活性位点包含Cys-184、Arg-197和His-120残基。反应产物的LC-MS/MS分析表明Cys-184被修饰为半胱氨酸磺酸(+48 amu)。从DTNB测定获得的结果支持Cys-184残基的氧化。LC-MS/MS还表明含Arg-197的肽被氧化。进行二维核磁共振分析以评估His-120可能的氧化情况,然而未观察到氧化现象。这些化合物具有通过氧化修饰底物结合所需的必需残基而使SrtA不可逆失活的潜力。