从分子理解到 N-端乙酰转移酶的机体生物学。
From Molecular Understanding to Organismal Biology of N-Terminal Acetyltransferases.
机构信息
Institute for Basic Research in Developmental Disabilities (IBR), Staten Island, NY 10314, USA; Biology PhD Program, The Graduate Center, The City University of New York, NY 10016, USA.
出版信息
Structure. 2019 Jul 2;27(7):1053-1055. doi: 10.1016/j.str.2019.06.002.
Abstract
In this issue of Structure, Deng et al. (2019) determine the structure of the yeast N-terminal acetyltransferases Naa10 and Naa50 in complex with Naa15 and demonstrate that Naa50 has negligible catalytic activity on its own but modulates Naa10/Naa15. This study provides insights into mechanisms involving amino-terminal acetylation of proteins.
摘要
在本期《结构》中，邓等人（2019）确定了酵母 N 端乙酰转移酶 Naa10 和 Naa50 与 Naa15 复合物的结构，并证实 Naa50 自身几乎没有催化活性，但能调节 Naa10/Naa15。这项研究为涉及蛋白质氨基端乙酰化的机制提供了新的见解。
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本文引用的文献
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Structure. 2019 Jul 2;27(7):1057-1070.e4. doi: 10.1016/j.str.2019.04.014. Epub 2019 May 30.
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Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15.NAA10 和 NAA15 变异个体的国际队列的表型和生化分析。
Hum Mol Genet. 2019 Sep 1;28(17):2900-2919. doi: 10.1093/hmg/ddz111.
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Co-translational, Post-translational, and Non-catalytic Roles of N-Terminal Acetyltransferases.N-末端乙酰转移酶的共翻译、翻译后及非催化作用
Mol Cell. 2019 Mar 21;73(6):1097-1114. doi: 10.1016/j.molcel.2019.02.007. Epub 2019 Mar 13.
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NAA10-related syndrome.NAA10 相关综合征。
Exp Mol Med. 2018 Jul 27;50(7):1-10. doi: 10.1038/s12276-018-0098-x.
5
Structure of Human NatA and Its Regulation by the Huntingtin Interacting Protein HYPK.人源 NatA 的结构及其被 Huntingtin 相互作用蛋白 HYPK 的调控。
Structure. 2018 Jul 3;26(7):925-935.e8. doi: 10.1016/j.str.2018.04.003. Epub 2018 May 10.
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N-terminal acetylome analysis reveals the specificity of Naa50 (Nat5) and suggests a kinetic competition between N-terminal acetyltransferases and methionine aminopeptidases.N 端乙酰化组分析揭示了 Naa50（Nat5）的特异性，并提示 N 端乙酰转移酶与甲硫氨酸氨肽酶之间存在动力学竞争。
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Loss of amino-terminal acetylation suppresses a prion phenotype by modulating global protein folding.氨基末端乙酰化的缺失通过调节整体蛋白质折叠来抑制朊病毒表型。
Nat Commun. 2014 Jul 15;5:4383. doi: 10.1038/ncomms5383.
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