학회소개 
| 한국분자·세포생물학회 학술상 생명과학상 수상자 | |
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김은준 (한국과학기술원 생명과학과)
Dr. Eunjoon Kim is a professor in the Department of Biological Sciences at KAIST. He received his bachelor's degree at Busan National University, master's degree at KAIST, and Ph.D. degree at Michigan State University. During PhD course, Dr. Kim characterized a potassium channel gene from the human parasite Schistosome under the guidance of Dr. James Bennett. During postdoctoral training, Dr. Kim characterized scaffolding proteins at excitatory synapses in the laboratory of Dr. Morgan Sheng at Harvard Medical School. Since he returned to Korea in 1997, he has explored the mechanisms underlying synapse formation and identified a large number of excitatory synaptic proteins. More recently, he has expanded his research towards the area of brain dysfunctions caused by defective synaptic proteins including autism, attention deficit/hyperactivity disorder (ADHD), schizophrenia, intellectual disability, and emotional disturbances. He is currently serving as an associate editor of Molecules and Cells, and an editorial board member for eLife, NeuroSignals, Experimental Neurobiology, Molecular Brain, and Frontiers in Molecular Neuroscience. He has recently been appointed as the director of the Center for Synaptic Brain Dysfunctions at the Institute for Basic Science (IBS), which is based at KAIST and will be organized by inviting about four senior group leaders for synergistic researches. Representative papers - Autistic-like social behavior in Shank2-mutant mice improved by restoring NMDA receptor function (2012). Nature 486, 261-265. - GIT1 is associated with attention deficit/hyperactivity disorder (ADHD) and ADHD-like behaviors in mice (2011). Nat. Med. 17, 566-572. - Trans-synaptic adhesion between NGL-3 and LAR regulates the formation of excitatory synapses (2009). Nat. Neurosci. 12, 428-437. - Regulated RalBP1 binding to RalA and PSD-95 controls AMPA receptor endocytosis and LTD (2009). PLoS Biol. 7, e1000187. - NGL family PSD-95-interacting adhesion molecules regulate excitatory synapse formation (2006). Nat. Neurosci. 9, 1294-1231. |
| 한국분자·세포생물학회 학술상 Molecules and Cells (M&C) 우수논문상 수상자 | |
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김권섭 (전남대학교 약학대학) 수상 논문 Regulation of Notch1/NICD and Hes1 expressions by GSK-3alpha/beta. (2009). Mol. Cells 27, 15-19. Notch signaling is controlled at multiple levels. In particular, stabilized Notch receptor activation directly affects the transcriptional activations of Notch target genes. Although some progress has been made in terms of defining the regulatory mechanism that alters Notch stability, it has not been determined whether Notch1/NICD stability is regulated by GSK-3a. Here, we show that Notch1/NICD levels are significantly regulated by GSK-3b and by GSK-3a. Treatment with LiCl (a specific GSK-3 inhibitor) or the overexpression of the kinase-inactive forms of GSK-3a/b significantly increased Notch1/NICD levels. Endogenous NICD levels were also increased by either GSK-3a/b- or GSK-3a-specific siRNA. Furthermore, it was found that GSK-3a binds to Notch1. Deletion analysis showed that at least three Thr residues in Notch1 (Thr-1851, 2123, and 2125) are critical for its response to LiCl, which increased not only the transcriptional activity of endogenous NICD but also Hes1 mRNA levels. Taken together, our results indicate that GSK-3a is a negative regulator of Notch1/NICD. |