Cell：首尔大学教授发现促进形成长期记忆的蛋白质

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Cell：首尔大学教授发现促进形成长期记忆的蛋白质 5月18日，韩国首尔大学姜奉均（音译）教授宣布发现促进形成长时记忆的蛋白质。生物的记忆主要分为持续1-2小时的短时记忆和通过反复学习能够持续24小时以上的长时记忆。在形成长时记忆方面，蛋白质合成和基因表达均不可或缺。姜奉均领导的科研组在传达外界刺激的神经体系中发现了存在于神经键内被称为“CAMAP”的蛋白质，该蛋白质将学习信号传达到细胞核后，合成能够形成长时记忆的蛋白质。科研组针对海兔进行实验的结
  生物谷报道：5月18日，韩国首尔大学姜奉均（音译）教授宣布发现促进形成长时记忆的蛋白质。  

姜奉均教授在世界上第一次发现“传递记忆信号逆行性转录因子”
  生物的记忆主要分为持续1-2小时的短时记忆和通过反复学习能够持续24小时以上的长时记忆。在形成长时记忆方面，蛋白质合成和基因表达均不可或缺。   
  姜奉均领导的科研组在传达外界刺激的神经体系中发现了存在于神经键内被称为“CAMAP”的蛋白质，该蛋白质将学习信号传达到细胞核后，合成能够形成长时记忆的蛋白质。  
  科研组针对海兔进行实验的结果，发现一种使细胞结合的粘附蛋白质——“CAMAP”起到了将信号从神经键传达到细胞核的传达作用。同时，在细胞核中与其它蛋白质“CREB”结合，起到形成长时记忆所需的转录因子作用，并诱导基因表达。  
  如果反复刺激海兔的尾部，反应会变得敏感。考虑到高级动物也存在这种类似的现象，科研组预测如果人类反复听取英语单词，会长时间留在记忆之中。  
  科研组表示，在“外界刺激→神经键→细胞核→长时记忆蛋白子形成及基因表达”这一信号传达链中，确认了起到连接环作用的蛋白质性质。
原始出处:
Cell, Vol 129, 801-812, 18 May 2007
Article
Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia
Seung-Hee Lee,1,7 Chae-Seok Lim,1,7 Hyungju Park,1,7 Jin-A Lee,1 Jin-Hee Han,1 Hyoung Kim,1 Ye-Hwang Cheang,1 Sue-Hyun Lee,1 Yong-Seok Lee,1 Hyoung-Gon Ko,1 Dong-Hyuk Jang,1 Hyongkyu Kim,2 Maria C. Miniaci,6,8 Dusan Bartsch,3 Eunjoon Kim,4 Craig H. Bailey,6 Eric R. Kandel,5,6 and Bong-Kiun Kaang1,


1 Department of Biological Sciences, Institute of Molecular Biology and Genetics, RIO, College of Natural Sciences, Seoul National University, San 56-1 Silim-dong Gwanak-gu, Seoul 151-747, Korea2 College of Medicine, Chungbuk National University, Cheongju 361-763, Korea3 Department of Molecular Biology, Central Institute of Mental Health, Mannheim 68159, Germany4 Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea5 Howard Hughes Medical Institute, 1051 Riverside Drive, New York, NY 10032, USA6 New York State Psychiatric Institute, Kavli Institute for Brain Sciences, Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA

Corresponding author
Bong-Kiun Kaang
kaang@snu.ac.kr
Summary
Repeated pulses of serotonin (5-HT) induce long-term facilitation (LTF) of the synapses between sensory and motor neurons of the gill-withdrawal reflex in Aplysia. To explore how apCAM downregulation at the plasma membrane and CREB-mediated transcription in the nucleus, both of which are required for the formation of LTF, might relate to each other, we cloned an apCAM-associated protein (CAMAP) by yeast two-hybrid screening. We found that 5-HT signaling at the synapse activates PKA which in turn phosphorylates CAMAP to induce the dissociation of CAMAP from apCAM and the subsequent translocation of CAMAP into the nucleus of sensory neurons. In the nucleus, CAMAP acts as a transcriptional coactivator for CREB1 and is essential for the activation of ApC/EBP required for the initiation of LTF. Combined, our data suggest that CAMAP is a retrograde signaling component that translocates from activated synapses to the nucleus during synapse-specific LTF.