Campus Forschung, 2. OG Rm 02.0058, Institute of Immunology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246, Hamburg, Germany.
Amino Acids. 2011 Jul;41(2):257-69. doi: 10.1007/s00726-010-0676-2. Epub 2010 Jul 21.
Arginine adenosine-5'-diphosphoribosylation (ADP-ribosylation) is an enzyme-catalyzed, potentially reversible posttranslational modification, in which the ADP-ribose moiety is transferred from NAD(+) to the guanidino moiety of arginine. At 540 Da, ADP-ribose has the size of approximately five amino acid residues. In contrast to arginine, which, at neutral pH, is positively charged, ADP-ribose carries two negatively charged phosphate moieties. Arginine ADP-ribosylation, thus, causes a notable change in size and chemical property at the ADP-ribosylation site of the target protein. Often, this causes steric interference of the interaction of the target protein with binding partners, e.g. toxin-catalyzed ADP-ribosylation of actin at R177 sterically blocks actin polymerization. In case of the nucleotide-gated P2X7 ion channel, ADP-ribosylation at R125 in the vicinity of the ligand-binding site causes channel gating. Arginine-specific ADP-ribosyltransferases (ARTs) carry a characteristic R-S-EXE motif that distinguishes these enzymes from structurally related enzymes which catalyze ADP-ribosylation of other amino acid side chains, DNA, or small molecules. Arginine-specific ADP-ribosylation can be inhibited by small molecule arginine analogues such as agmatine or meta-iodobenzylguanidine (MIBG), which themselves can serve as targets for arginine-specific ARTs. ADP-ribosylarginine specific hydrolases (ARHs) can restore target protein function by hydrolytic removal of the entire ADP-ribose moiety. In some cases, ADP-ribosylarginine is processed into secondary posttranslational modifications, e.g. phosphoribosylarginine or ornithine. This review summarizes current knowledge on arginine-specific ADP-ribosylation, focussing on the methods available for its detection, its biological consequences, and the enzymes responsible for this modification and its reversal, and discusses future perspectives for research in this field.
精氨酸腺苷-5′-二磷酸核糖基化(ADP-核糖基化)是一种酶催化的、潜在可逆的翻译后修饰,其中 ADP-核糖部分从 NAD(+)转移到精氨酸的胍基部分。ADP-核糖的分子量为 540Da,大约相当于五个氨基酸残基的大小。与在中性 pH 值下带正电荷的精氨酸不同,ADP-核糖带有两个带负电荷的磷酸部分。因此,精氨酸 ADP-核糖基化会导致靶蛋白 ADP-核糖基化位点的大小和化学性质发生显著变化。通常,这会导致靶蛋白与结合伴侣相互作用的空间位阻,例如毒素催化的肌动蛋白 R177 的 ADP-核糖基化会阻止肌动蛋白聚合。在核苷酸门控 P2X7 离子通道的情况下,靠近配体结合位点的 R125 处的 ADP-核糖基化会引起通道门控。精氨酸特异性 ADP-核糖基转移酶(ARTs)携带一个特征性的 R-S-EXE 基序,该基序将这些酶与结构上相关的酶区分开来,后者催化其他氨基酸侧链、DNA 或小分子的 ADP-核糖基化。精氨酸特异性 ADP-核糖基化可以被小分子精氨酸类似物如胍丁胺或间碘苄胍(MIBG)抑制,这些类似物本身可以作为精氨酸特异性 ARTs 的靶标。ADP-核糖基精氨酸特异性水解酶(ARHs)可以通过水解去除整个 ADP-核糖部分来恢复靶蛋白的功能。在某些情况下,ADP-核糖基精氨酸会被加工成次级翻译后修饰,例如磷酸核糖基精氨酸或鸟氨酸。本综述总结了精氨酸特异性 ADP-核糖基化的最新知识,重点介绍了其检测方法、生物学后果以及负责这种修饰及其逆转的酶,并讨论了该领域未来的研究前景。