不同的试验间隔揭示了NTAN1基因缺陷小鼠在时间上定义的记忆缺陷和增强。
Varying intertrial interval reveals temporally defined memory deficits and enhancements in NTAN1-deficient mice.
作者信息
Balogh S A, Kwon Y T, Denenberg V H
机构信息
Biobehavioral Sciences Graduate Degree Program, University of Connecticut, Storrs, Connecticut 06269, USA.
出版信息
Learn Mem. 2000 Sep-Oct;7(5):279-86. doi: 10.1101/lm.33500.
Abstract
The N-end rule is one ubiquitin-proteolytic pathway that relates the in vivo half-life of a protein to the identity of its N-terminal residue. NTAN1 deamidates N-terminal asparagine to aspartate, which is conjugated to arginine by ATE1. An N-terminal arginine-bearing substrate protein is recognized, ubiquitylated by UBR1/E3alpha, and subsequently degraded by 26S proteasomes. Previous research showed that NTAN1-deficient mice exhibited impaired long-term memory in the Lashley III maze. Therefore, a series of studies, designed to assess the role of NTAN1 in short- and intermediate-term memory processes, was undertaken. Two hundred sixty mice (126 -/-; 134 +/ +) received Lashley III maze training with intertrial intervals ranging from 2-180 min. Results indicated that inactivation of NTAN1 amidase differentially affects short-, intermediate-, and long-term memory.
摘要
N端规则是一种泛素-蛋白水解途径，它将蛋白质在体内的半衰期与其N端残基的身份联系起来。NTAN1将N端天冬酰胺脱酰胺化为天冬氨酸，后者由ATE1与精氨酸缀合。携带N端精氨酸的底物蛋白被识别，由UBR1/E3α进行泛素化，随后被26S蛋白酶体降解。先前的研究表明，NTAN1缺陷小鼠在拉什利三世迷宫中表现出长期记忆受损。因此，开展了一系列旨在评估NTAN1在短期和中期记忆过程中作用的研究。260只小鼠（126只基因敲除小鼠；134只野生型小鼠）接受了拉什利三世迷宫训练，试验间隔时间为2至180分钟。结果表明，NTAN1酰胺酶的失活对短期、中期和长期记忆有不同影响。
相似文献
1
Varying intertrial interval reveals temporally defined memory deficits and enhancements in NTAN1-deficient mice.不同的试验间隔揭示了NTAN1基因缺陷小鼠在时间上定义的记忆缺陷和增强。
Learn Mem. 2000 Sep-Oct;7(5):279-86. doi: 10.1101/lm.33500.
2
Facilitated stimulus-response associative learning and long-term memory in mice lacking the NTAN1 amidase of the N-end rule pathway.缺乏N端规则途径的NTAN1酰胺酶的小鼠中易化的刺激-反应联想学习和长期记忆。
Brain Res. 2001 Feb 23;892(2):336-43. doi: 10.1016/s0006-8993(00)03268-6.
3
Altered activity, social behavior, and spatial memory in mice lacking the NTAN1p amidase and the asparagine branch of the N-end rule pathway.缺乏NTAN1p酰胺酶和N端规则途径天冬酰胺分支的小鼠的活动、社会行为和空间记忆改变。
Mol Cell Biol. 2000 Jun;20(11):4135-48. doi: 10.1128/MCB.20.11.4135-4148.2000.
4
Behavioral characterization of mice lacking the ubiquitin ligase UBR1 of the N-end rule pathway.缺乏N端规则途径泛素连接酶UBR1的小鼠的行为特征
Genes Brain Behav. 2002 Nov;1(4):223-9. doi: 10.1034/j.1601-183x.2002.10404.x.
5
A mouse amidase specific for N-terminal asparagine. The gene, the enzyme, and their function in the N-end rule pathway.一种对N端天冬酰胺具有特异性的小鼠酰胺酶。该基因、酶及其在N端规则途径中的功能。
J Biol Chem. 1996 Nov 8;271(45):28521-32. doi: 10.1074/jbc.271.45.28521.
6
Construction and analysis of mouse strains lacking the ubiquitin ligase UBR1 (E3alpha) of the N-end rule pathway.缺乏N端规则途径泛素连接酶UBR1（E3α）的小鼠品系的构建与分析。
Mol Cell Biol. 2001 Dec;21(23):8007-21. doi: 10.1128/MCB.21.23.8007-8021.2001.
7
Stimulation of ubiquitin-proteasome pathway through the expression of amidohydrolase for N-terminal asparagine (Ntan1) in cultured rat hippocampal neurons exposed to static magnetism.在暴露于静磁场的培养大鼠海马神经元中，通过N-末端天冬酰胺酶（Ntan1）的表达刺激泛素-蛋白酶体途径。
J Neurochem. 2006 Mar;96(6):1519-30. doi: 10.1111/j.1471-4159.2006.03655.x.
8
Structural Analyses on the Deamidation of N-Terminal Asn in the Human N-Degron Pathway.结构分析人 N-去稳定化途径中 N 端天冬酰胺的脱酰胺作用。
Biomolecules. 2020 Jan 20;10(1):163. doi: 10.3390/biom10010163.
9
Working memory deficits in retinoid X receptor gamma-deficient mice.维甲酸X受体γ缺陷小鼠的工作记忆缺陷
Learn Mem. 2005 May-Jun;12(3):318-26. doi: 10.1101/lm.89805. Epub 2005 May 16.
10
Expression and biochemical characterization of the human enzyme N-terminal asparagine amidohydrolase.人源酶 N-端天门冬酰胺酰胺水解酶的表达和生化特性分析。
Biochemistry. 2011 Apr 12;50(14):3025-33. doi: 10.1021/bi101832w. Epub 2011 Mar 18.
引用本文的文献
1
16p13.11 deletion variants associated with neuropsychiatric disorders cause morphological and synaptic changes in induced pluripotent stem cell-derived neurons.与神经精神疾病相关的16p13.11缺失变异导致诱导多能干细胞衍生神经元的形态和突触变化。
Front Psychiatry. 2022 Nov 3;13:924956. doi: 10.3389/fpsyt.2022.924956. eCollection 2022.
2
The Ntan1 gene is expressed in perineural glia and neurons of adult Drosophila.Ntan1 基因在成年果蝇的神经周围胶质细胞和神经元中表达。
Sci Rep. 2022 Aug 30;12(1):14749. doi: 10.1038/s41598-022-18999-8.
3
Structural Analyses on the Deamidation of N-Terminal Asn in the Human N-Degron Pathway.结构分析人 N-去稳定化途径中 N 端天冬酰胺的脱酰胺作用。
Biomolecules. 2020 Jan 20;10(1):163. doi: 10.3390/biom10010163.
4
Alzheimer's associated amyloid and tau deposition co-localizes with a homeostatic myelin repair pathway in two mouse models of post-stroke mixed dementia.阿尔茨海默病相关的淀粉样蛋白和tau 沉积与两种卒中后混合性痴呆小鼠模型中的稳态髓鞘修复途径共存。
Acta Neuropathol Commun. 2018 Sep 24;6(1):100. doi: 10.1186/s40478-018-0603-4.
5
A picorna-like virus suppresses the N-end rule pathway to inhibit apoptosis.一种类微小 RNA 病毒通过抑制 N 末端规则途径来抑制细胞凋亡。
Elife. 2017 Dec 12;6:e30590. doi: 10.7554/eLife.30590.
6
p62/SQSTM1/Sequestosome-1 is an N-recognin of the N-end rule pathway which modulates autophagosome biogenesis.p62/SQSTM1/聚集体蛋白1是N端规则途径的一种N识别蛋白，可调节自噬体的生物发生。
Nat Commun. 2017 Jul 24;8(1):102. doi: 10.1038/s41467-017-00085-7.
7
Protein Quality Control by Molecular Chaperones in Neurodegeneration.神经退行性变中分子伴侣介导的蛋白质质量控制
Front Neurosci. 2017 Apr 6;11:185. doi: 10.3389/fnins.2017.00185. eCollection 2017.
8
NDE1 and NDEL1 from genes to (mal)functions: parallel but distinct roles impacting on neurodevelopmental disorders and psychiatric illness.从基因到（异常）功能的NDE1和NDEL1：影响神经发育障碍和精神疾病的平行但不同的作用
Cell Mol Life Sci. 2017 Apr;74(7):1191-1210. doi: 10.1007/s00018-016-2395-7. Epub 2016 Oct 14.
9
Concomitant deletion of chromosome 16p13.11 and triplication of chromosome 19p13.3 in a child with developmental disorders, intellectual disability, and epilepsy.一名患有发育障碍、智力残疾和癫痫的儿童同时存在16号染色体p13.11区域缺失和19号染色体p13.3区域三倍体异常。
Mol Cytogenet. 2015 Feb 5;8:9. doi: 10.1186/s13039-015-0115-x. eCollection 2015.
10
Gene expression patterns in the hippocampus during the development and aging of Glud1 (Glutamate Dehydrogenase 1) transgenic and wild type mice.在 Glud1（谷氨酸脱氢酶 1）转基因和野生型小鼠的发育和衰老过程中海马中的基因表达模式。
BMC Neurosci. 2014 Mar 4;15:37. doi: 10.1186/1471-2202-15-37.
本文引用的文献
1
Nuclear RNA changes of nerve cells during a learning experiment in rats.大鼠学习实验期间神经细胞核RNA的变化
Proc Natl Acad Sci U S A. 1962 Aug;48(8):1366-73. doi: 10.1073/pnas.48.8.1366.
2
THE INFLUENCE OF ACTINOMYCIN-D ON BRAIN RNA SYNTHESIS AND ON MEMORY.
J Neurochem. 1964 Mar;11:187-95. doi: 10.1111/j.1471-4159.1964.tb06128.x.
3
The molecular basis of memory and learning.
Psychol Rev. 1962 Nov;69:537-41. doi: 10.1037/h0045270.
4
Is memory a matter of enzyme induction?
Science. 1962 Nov 23;138(3543):889-90. doi: 10.1126/science.138.3543.889.
5
Retention of an incompletely learned avoidance response: some further analyses.对未完全学会的回避反应的保持：一些进一步的分析
J Comp Physiol Psychol. 1963 Aug;56:713-8. doi: 10.1037/h0043941.
6
The retention of an incompletely learned avoidance response.对未完全学会的回避反应的保持。
J Comp Physiol Psychol. 1957 Oct;50(5):457-60. doi: 10.1037/h0044226.
7
Memory decrement produced by ECS as a function of distribution in original learning.由电休克惊厥（ECS）产生的记忆减退作为原始学习中分布的函数。
J Comp Physiol Psychol. 1957 Aug;50(4):401-4. doi: 10.1037/h0042901.
8
Evolution proposes and ontogeny disposes.
Brain Lang. 2000 Jun 15;73(2):274-96. doi: 10.1006/brln.2000.2307.
9
Altered activity, social behavior, and spatial memory in mice lacking the NTAN1p amidase and the asparagine branch of the N-end rule pathway.缺乏NTAN1p酰胺酶和N端规则途径天冬酰胺分支的小鼠的活动、社会行为和空间记忆改变。
Mol Cell Biol. 2000 Jun;20(11):4135-48. doi: 10.1128/MCB.20.11.4135-4148.2000.
Zotero 插件