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SNX14 is a bifunctional negative regulator for neuronal 5‐HT<sub>6</sub> receptor signaling
Ha, Chang Man,Park, Daehun,Kim, Yoonju,Na, Myeongsu,Panda, Surabhi,Won, Sehoon,Kim, Hyun,Ryu, Hoon,Park, Zee Yong,Rasenick, Mark M.,Chang, Sunghoe The Company of Biologists Limited 2015 Journal of cell science Vol.128 No.9
<P>The 5-hydroxytryptamine (5-HT, also known as serotonin) subtype 6 receptor (5-HT6R, also known as HTR6) plays roles in cognition, anxiety and learning and memory disorders, yet new details concerning its regulation remain poorly understood. In this study, we found that 5-HT6R directly interacted with SNX14 and that this interaction dramatically increased internalization and degradation of 5-HT6R. Knockdown of endogenous SNX14 had the opposite effect. SNX14 is highly expressed in the brain and contains a putative regulator of G-protein signaling (RGS) domain. Although its RGS domain was found to be non-functional as a GTPase activator for Gas, we found that it specifically bound to and sequestered Gas, thus inhibiting downstream cAMP production. We further found that protein kinase A (PKA)-mediated phosphorylation of SNX14 inhibited its binding to Gas and diverted SNX14 from Gas binding to 5-HT6R binding, thus facilitating the endocytic degradation of the receptor. Therefore, our results suggest that SNX14 is a dual endogenous negative regulator in 5-HT6R-mediated signaling pathway, modulating both signaling and trafficking of 5-HT6R.</P>
Kim, Yoonju,Ha, Chang Man,Chang, Sunghoe American Society for Biochemistry and Molecular Bi 2013 The Journal of biological chemistry Vol.288 No.41
<P>SNX26, a brain-enriched RhoGAP, plays a key role in dendritic arborization during early neuronal development in the neocortex. In mature neurons, it is localized to dendritic spines, but little is known about its role in later stages of development. Our results show that SNX26 interacts with PSD-95 in dendritic spines of cultured hippocampal neurons, and as a GTPase-activating protein for Cdc42, it decreased the F-actin content in COS-7 cells and in dendritic spines of neurons. Overexpression of SNX26 resulted in a GTPase-activating protein activity-dependent decrease in total protrusions and spine density together with dramatic inhibition of filopodia-to-spine transformations. Such effects of SNX26 were largely rescued by a constitutively active mutant of Cdc42. Consistently, an shRNA-mediated knockdown of SNX26 significantly increased total protrusions and spine density, resulting in an increase in thin or stubby type spines at the expense of the mushroom spine type. Moreover, endogenous expression of SNX26 was shown to be bi-directionally modulated by neuronal activity. Therefore, we propose that in addition to its key role in neuronal development, SNX26 also has a role in the activity-dependent structural change of dendritic spines in mature neurons.</P>
Kim, Yoonju,Lee, Sang-Eun,Park, Joohyun,Kim, Minhyung,Lee, Boyoon,Hwang, Daehee,Chang, Sunghoe American Society for Biochemistry and Molecular Bi 2015 The Journal of biological chemistry Vol.290 No.12
<P>Recent studies have reported conflicting results regarding the role of ARF6 in dendritic spine development, but no clear answer for the controversy has been suggested. We found that ADP-ribosylation factor 6 (ARF6) either positively or negatively regulates dendritic spine formation depending on neuronal maturation and activity. ARF6 activation increased the spine formation in developing neurons, whereas it decreased spine density in mature neurons. Genome-wide microarray analysis revealed that ARF6 activation in each stage leads to opposite patterns of expression of a subset of genes that are involved in neuronal morphology. ARF6-mediated Rac1 activation via the phospholipase D pathway is the coincident factor in both stages, but the antagonistic RhoA pathway becomes involved in the mature stage. Furthermore, blocking neuronal activity in developing neurons using tetrodotoxin or enhancing the activity in mature neurons using picrotoxin or chemical long term potentiation reversed the effect of ARF6 on each stage. Thus, activity-dependent dynamic changes in ARF6-mediated spine structures may play a role in structural plasticity of mature neurons.</P>
Overexpression of Dyrk1A Causes the Defects in Synaptic Vesicle Endocytosis
Kim, Yoonju,Park, Joohyun,Song, Woo-Joo,Chang, Sunghoe S. Karger AG 2011 Neuro-Signals Vol.18 No.3
<P>Trisomy 21-linked Dyrk1A (dual-specificity tyrosine phosphorylation-regulated kinase 1A) overexpression is implicated in pathogenic mechanisms underlying mental retardation in Down syndrome (DS). It is known to phosphorylate multiple substrates including endocytic proteins in vitro, but the functional consequence of Dyrk1A-mediated phosphorylation on endocytosis has never been investigated. Here, we show that overexpression of Dyrk1A causes defects in clathrin-mediated endocytosis and specifically, in the recruitment of endocytic proteins to clathrin-coated pits in fibroblasts. Synaptic vesicle endocytosis also significantly slowed down as a result of Dyrk1A overexpression in cultured hippocampal neurons. These effects are dependent on Dyrk1A kinase activity. The inhibitory effect of Dyrk1A on synaptic vesicle endocytosis was confirmed in neuronal cultures derived from transgenic mice overexpressing Dyrk1A at levels found in DS. Pharmacological blockade of Dyrk1A with epigallocatechin gallate rescued the endocytic phenotypes found in transgenic neurons. Together, our results suggest that aberrant Dyrk1A-mediated phosphorylation of the endocytic machinery perturbs synaptic vesicle endocytosis, which may contribute to synaptic dysfunctions and cognitive deficits associated with DS.</P><P>Copyright © 2010 S. Karger AG, Basel</P>
이질 망에서의 전송성능 향상을 위한 mSCTP 기반 수직 핸드오버 메커니즘
장문정(Moonjeong Chang),이미정(Meejeong Lee),이윤주(Yoonju Lee) 한국정보과학회 2006 한국정보과학회 학술발표논문집 Vol.33 No.1
오버레이 네트워크 환경에서 이동 사용자에게 최적의 서비스를 제공하기 위해서 효율적인 수직 핸드오버 기술은 필수적이다. 이에 본 논문에서는 비실시간 응용의 성능을 최대화할 수 있는 종단 간 이동성 지원 방안을 기반으로 한 수직 핸드오버 메커니즘을 제안하였다. 본 논문의 특징은 먼저 수직 핸드오버 트리거링 방법과 수직 핸드오버 결정 규칙을 정의하였고, 비실시간 응용의 성능을 최대화하는 새로운 혼잡제어 메커니즘을 제안하였다. 마지막으로 핑퐁 현상이 전송성능에 미치는 영향을 줄이기 위하여 stability period 정의하였다. 추후 시뮬레이션을 통해 제안하는 방안의 성능을 평가하고자 한다.
비디오 스트리밍 서비스를 위한 mSCTP 기반 수직 핸드오버 메커니즘
장문정(Moonjeong Chang),이미정(Meejeong Lee),이윤주(Yoonju Lee) 한국정보과학회 2006 한국정보과학회 학술발표논문집 Vol.33 No.1
본 논문에서는 오버레이 네트워크 환경에서 비디오 스트리밍 서비스의 성능을 향상시키기 위한 수직 핸드오버 메커니즘을 제안한다. 본 논문에서는 error propagation 문제를 완화함으로써 비디오 스트리밍 서비스의 성능을 향상시킨다. 이를 위해 프레임들의 전송 경로를 유형별로 분리하고, 프레임들의 손실률을 최소화하는 재전송 정책을 사용하며, forced 수직 핸드오버 시 멀티캐스팅 방법을 사용하였다. 또한 stability period 정의하여 핑퐁 현상이 전송성능에 미치는 영향을 줄였다. 시뮬레이션을 통해 제안하는 방안이 error propagation 문제를 개선함으로써 이동 사용자에게 끊김없는 비디오 스트리밍 서비스를 제공함을 알 수 있었다.
2018 Guidelines for the management of dyslipidemia in Korea
( Eun-Jung Rhee ),( Hyeon Chang Kim ),( Jae Hyeon Kim ),( Eun Young Lee ),( Byung Jin Kim ),( Eun Mi Kim ),( YoonJu Song ),( Jeong Hyun Lim ),( Hae Jin Kim ),( Seonghoon Choi ),( Min Kyong Moon ),( Ji 대한내과학회 2019 The Korean Journal of Internal Medicine Vol.34 No.5
SCAMP5 Plays a Critical Role in Synaptic Vesicle Endocytosis during High Neuronal Activity
Zhao, Haiyan,Kim, Yoonju,Park, Joohyun,Park, Daehun,Lee, Sang-Eun,Chang, Iree,Chang, Sunghoe Society for Neuroscience 2014 The Journal of neuroscience Vol.34 No.30
<P>Secretory carrier membrane protein 5 (SCAMP5), a recently identified candidate gene for autism, is brain specific and highly abundant in synaptic vesicles (SVs), but its function is currently unknown. Here, we found that knockdown (KD) of endogenous SCAMP5 by SCAMP5-specific shRNAs in cultured rat hippocampal neurons resulted in a reduction in total vesicle pool size as well as in recycling pool size, but the recycling/resting pool ratio was significantly increased. SCAMP5 KD slowed endocytosis after stimulation, but impaired it severely during strong stimulation. We also found that KD dramatically lowered the threshold of activity at which SV endocytosis became unable to compensate for the ongoing exocytosis occurring during a stimulus. Reintroducing shRNA-resistant SCAMP5 reversed these endocytic defects. Therefore, our results suggest that SCAMP5 functions during high neuronal activity when a heavy load is imposed on endocytosis. Our data also raise the possibility that the reduction in expression of SCAMP5 in autistic patients may be related to the synaptic dysfunction observed in autism.</P>
nArgBP2 regulates excitatory synapse formation by controlling dendritic spine morphology
Lee, Sang-Eun,Kim, Yoonju,Han, Jeong-Kyu,Park, Hoyong,Lee, Unghwi,Na, Myeongsu,Jeong, Soomin,Chung, ChiHye,Cestra, Gianluca,Chang, Sunghoe National Academy of Sciences 2016 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.113 No.24
<P>Neural Abelson-related gene-binding protein 2 (nArgBP2) was originally identified as a protein that directly interacts with synapseassociated protein 90/postsynaptic density protein 95-associated protein 3 (SAPAP3), a postsynaptic scaffolding protein critical for the assembly of glutamatergic synapses. Although genetic deletion of nArgBP2 in mice leads to manic/bipolar-like behaviors resembling many aspects of symptoms in patients with bipolar disorder, the actual function of nArgBP2 at the synapse is completely unknown. Here, we found that the knockdown (KD) of nArgBP2 by specific small hairpin RNAs (shRNAs) resulted in a dramatic change in dendritic spine morphology. Reintroducing shRNA-resistant nArgBP2 reversed these defects. In particular, nArgBP2 KD impaired spinesynapse formation such that excitatory synapses terminated mostly at dendritic shafts instead of spine heads in spiny neurons, although inhibitory synapse formation was not affected. nArgBP2 KD further caused a marked increase of actin cytoskeleton dynamics in spines, which was associated with increased Wiskott-Aldrich syndrome protein-family verprolin homologous protein 1 (WAVE1)/p21-activated kinase (PAK) phosphorylation and reduced activity of cofilin. These effects of nArgBP2 KD in spines were rescued by inhibiting PAK or activating cofilin combined with sequestration of WAVE. Together, our results suggest that nArgBP2 functions to regulate spine morphogenesis and subsequent spine-synapse formation at glutamatergic synapses. They also raise the possibility that the aberrant regulation of synaptic actin filaments caused by reduced nArgBP2 expression may contribute to the manifestation of the synaptic dysfunction observed in manic/bipolar disorder.</P>
Chung, Young-Seek,Lee, Yoonju,So, Joonho,Kim, Joonyeon,Cheon, Chang-Yul,Lee, Byungje,Sarkar, Tapan K. Wiley Subscription Services, Inc., A Wiley Company 2007 MICROWAVE AND OPTICAL TECHNOLOGY LETTERS Vol.49 No.11
<P>In this article, we propose a new stable solution for the time domain electric field integral equation (TD-EFIE) for arbitrarily shaped conducting structures, which utilizes weighted Laguerre polynomials as temporal basis functions, which means that the unknown surface currents are expanded by these basis functions. The proposed algorithm is based on the Galerkin's scheme that involves separate spatial and temporal testing procedures. By introducing the temporal testing procedure, the conventional marching-on in time procedure can be replaced by a recursive relation between the different orders of the weighted Laguerre polynomials. In this article, by deriving the integral formulation using the weighted Laguerre polynomials, we solve for the surface current density as the unknown directly. To verify the accuracy of the proposed method, we have compared the results with the inverse discrete Fourier transform of the frequency domain solutions for the electric field integral equation. © 2007 Wiley Periodicals, Inc. Microwave Opt Technol Lett 49: 2789–2793, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.22835</P>