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Regulation of dendritic arborization by BCR Rac1 GTPase-activating protein, a substrate of PTPRT.
Park, A-Reum,Oh, Daeyoung,Lim, So-Hee,Choi, Jeonghoon,Moon, Jeonghee,Yu, Dae-Yeol,Park, Sung Goo,Heisterkamp, Nora,Kim, Eunjoon,Myung, Pyung-Keun,Lee, Jae-Ran Cambridge University Press 2012 Journal of cell science Vol.125 No.19
<P>Dendritic arborization is important for neuronal development as well as the formation of neural circuits. Rac1 is a member of the Rho GTPase family that serve as regulators of neuronal development. Breakpoint cluster region protein (BCR) is a Rac1 GTPase-activating protein that is abundantly expressed in the central nervous system. Here, we show that BCR plays a key role in neuronal development. Dendritic arborization and actin polymerization were attenuated by overexpression of BCR in hippocampal neurons. Knockdown of BCR using specific shRNAs increased the dendritic arborization as well as actin polymerization. The number of dendrites in null mutant BCR(-/-) mice was considerably increased compared with that in wild-type mice. We found that the function of the BCR GTPase-activating domain could be modulated by protein tyrosine phosphatase receptor T (PTPRT), which is expressed principally in the brain. We demonstrate that tyrosine 177 of BCR was the main target of PTPRT and the BCR mutant mimicking dephosphorylation of tyrosine 177 alleviated the attenuation of dendritic arborization. Additionally the attenuated dendritic arborization found upon BCR overexpression was relieved upon co-expression of PTPRT. When PTPRT was knocked down by a specific shRNA, the dendritic arborization was significantly reduced. The activity of the BCR GTPase-activating domain was modulated by means of conversions between the intra- and inter-molecular interactions, which are finely regulated through the dephosphorylation of a specific tyrosine residue by PTPRT. We thus show conclusively that BCR is a novel substrate of PTPRT and that BCR is involved in the regulation of neuronal development via control of the BCR GTPase-activating domain function by PTPRT.</P>
Eunjoon Park,Jina Park,Cheol-Hong Cheon 대한화학회 2021 Bulletin of the Korean Chemical Society Vol.42 No.3
A different reactivity between cyanide and NHC with 4-(2-formylphenoxy) but-2-enoate derivatives is described.
Cheolho Park,Namhyun Kang,Stephen Liu,Juseung Lee,Eunjoon Chun,Sun‑Joon Yoo 대한금속·재료학회 2019 METALS AND MATERIALS International Vol.25 No.3
Hydrogen can provide pure and clean energy; however, to use it as an energy source, facilities such as hydrogen carriersand recharging stations need to be constructed. Structural steels are affected by hydrogen embrittlement (HE), and theirsusceptibility to this needs to be investigated prior to their use in construction. Most structural steels are normally fabricatedusing thermomechanical controlled processing, which produces a large dislocation density to increase strength. This studyinvestigated the prestrain effect on HE susceptibility of EH 36 steels using thermal desorption spectroscopy (TDS) andin situ slow-strain-rate testing. Hydrogen was electrochemically charged into specimens, and the reversible hydrogen contentand that relating to trap sites were measured using TDS. With an increase in prestrain, there was increase in the diffusiblehydrogen content; furthermore, with hydrogen charging, there was a drastic reduction in total elongation with an increasein prestrain. In addition, there was an increase in HE susceptibility with an increase in prestrain compared to when an aircondition was employed. Specifically, there was an abrupt increase in HE sensitivity at a prestrain value between 10 and15%; strain hardening was more dominant below a prestrain value of 10%; and HE was more dominant above a prestrainvalue of 15% for EH 36 steels.
Yoo, Taesun,Cho, Heejin,Lee, Jiseok,Park, Haram,Yoo, Ye-Eun,Yang, Esther,Kim, Jin Yong,Kim, Hyun,Kim, Eunjoon Frontiers Media S.A. 2018 Frontiers in cellular neuroscience Vol.12 No.-
<P>Shank3 is an excitatory postsynaptic scaffolding protein implicated in multiple brain disorders, including autism spectrum disorders (ASD) and Phelan-McDermid syndrome (PMS). Although previous neurobiological studies on Shank3 and <I>Shank3</I>-mutant mice have revealed diverse roles of Shank3 in the regulation of synaptic, neuronal and brain functions, whether Shank3 expression in specific cell types distinctly contributes to mouse phenotypes remains largely unclear. In the present study, we generated two <I>Shank3</I>-mutant mouse lines (exons 14–16) carrying global and GABA neuron-specific deletions and characterized their electrophysiological and behavioral phenotypes. These mouse lines show similar decreases in excitatory synaptic input onto dorsolateral striatal neurons. In addition, the abnormal social and locomotor behaviors observed in global <I>Shank3</I>-mutant mice are strongly mimicked by GABA neuron-specific <I>Shank3</I>-mutant mice, whereas the repetitive and anxiety-like behaviors are only partially mimicked. These results suggest that GABAergic <I>Shank3</I> (exons 14–16) deletion has strong influences on striatal excitatory synaptic transmission and social and locomotor behaviors in mice.</P>
Um, Ji Won,Choii, Gayoung,Park, Dongseok,Kim, Dongwook,Jeon, Sangmin,Kang, Hyeyeon,Mori, Takuma,Papadopoulos, Theofilos,Yoo, Taesun,Lee, Yeunkum,Kim, Eunjoon,Tabuchi, Katsuhiko,Ko, Jaewon American Society for Biochemistry and Molecular Bi 2016 The Journal of biological chemistry Vol.291 No.19
<P>Gephyrin is a central scaffold protein that mediates development, function, and plasticity of mammalian inhibitory synapses by interacting with various inhibitory synaptic proteins. Here, we show that IQSLC3, a guanine nucleotide exchange factor for ARE6, directly interacts with gephyrin, an interaction that is critical for the inhibitory synapse localization of IQSEC3. Overexpression of IQSEC3 increases inhibitory, but not excitatory, synapse density in a guanine nucleotide exchange factor activity-dependent manner. Conversely, knockdown of IQSEC3 decreases size of gephyrin cluster without altering gephyrin puncta density. Collectively, these data reveal that IQSEC3 acts together with gephyrin to regulate inhibitory synapse development.</P>
Kim, Jung A,Kim, Doyoun,Won, Seoung Youn,Han, Kyung Ah,Park, Dongseok,Cho, Eunju,Yun, Nayoung,An, Hyun Joo,Um, Ji Won,Kim, Eunjoon,Lee, Jie-Oh,Ko, Jaewon,Kim, Ho Min Elsevier 2017 Neuron Vol.94 No.6
<P><B>Summary</B></P> <P>Membrane-associated mucin domain-containing glycosylphosphatidylinositol anchor proteins (MDGAs) bind directly to neuroligin-1 (NL1) and neuroligin-2 (NL2), thereby respectively regulating excitatory and inhibitory synapse development. However, the mechanisms by which MDGAs modulate NL activity to specify development of the two synapse types remain unclear. Here, we determined the crystal structures of human NL2/MDGA1 Ig1-3 complex, revealing their stable 2:2 arrangement with three interaction interfaces. Cell-based assays using structure-guided, site-directed MDGA1 mutants showed that all three contact patches were required for the MDGA’s negative regulation of NL2-mediated synaptogenic activity. Furthermore, MDGA1 competed with neurexins for NL2 via its Ig1 domain. The binding affinities of both MDGA1 and MDGA2 for NL1 and NL2 were similar, consistent with the structural prediction of similar binding interfaces. However, MDGA1 selectively associated with NL2, but not NL1, in vivo. These findings collectively provide structural insights into the mechanism by which MDGAs negatively modulate synapse development governed by NLs/neurexins.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Crystal structure of neuroligin-2 (NL2) in complex with MDGA1 Ig1-Ig3 domains </LI> <LI> MDGA1 Ig1-Ig2 domains interact with NL2 dimer with 2:2 stoichiometry </LI> <LI> MDGA1 competes with Nrx1β for NL2 binding via their overlapping binding site on NL2 </LI> <LI> MDGA1 selectively forms complexes with NL2, but not NL1, in vivo </LI> </UL> </P>
Choi, Su-Yeon,Han, Kihoon,Cutforth, Tyler,Chung, Woosuk,Park, Haram,Lee, Dongsoo,Kim, Ryunhee,Kim, Myeong-Heui,Choi, Yeeun,Shen, Kang,Kim, Eunjoon Frontiers Media S.A. 2015 Frontiers in cellular neuroscience Vol.9 No.-
<P>Synaptic adhesion molecules regulate diverse aspects of neuronal synapse development, including synapse specificity, formation, and maturation. Neph2, also known as Kirrel3, is an immunoglobulin superfamily adhesion molecule implicated in intellectual disability, neurocognitive delay associated with Jacobsen syndrome, and autism spectrum disorders. We here report mice lacking Neph2 (<I>Neph2<SUP>-/-</SUP></I> mice) display moderate hyperactivity in a familiar, but not novel, environment and defective novel object recognition with normal performances in Morris water maze spatial learning and memory, contextual fear conditioning and extinction, and pattern separation tests. These mice also show normal levels of anxiety-like behaviors, social interaction, and repetitive behaviors. At the synapse level, <I>Neph2<SUP>-/-</SUP></I> dentate gyrus granule cells exhibit unaltered dendritic spine density and spontaneous excitatory synaptic transmission. These results suggest that Neph2 is important for normal locomotor activity and object recognition memory.</P>
Lee, Seungjoon,Lee, Eunee,Kim, Ryunhee,Kim, Jihye,Lee, Suho,Park, Haram,Yang, Esther,Kim, Hyun,Kim, Eunjoon Frontiers Media S.A. 2018 Frontiers in molecular neuroscience Vol.11 No.-
<P>Shank2 is an abundant postsynaptic scaffolding protein implicated in neurodevelopmental and psychiatric disorders, including autism spectrum disorders (ASD). Deletion of <I>Shank2</I> in mice has been shown to induce social deficits, repetitive behaviors, and hyperactivity, but the identity of the cell types that contribute to these phenotypes has remained unclear. Here, we report a conditional mouse line with a <I>Shank2</I> deletion restricted to parvalbumin (PV)-positive neurons (<I>Pv-Cre;Shank2</I><SUP>fl/fl</SUP> mice). These mice display moderate hyperactivity in both novel and familiar environments and enhanced self-grooming in novel, but not familiar, environments. In contrast, they showed normal levels of social interaction, anxiety-like behavior, and learning and memory. Basal brain rhythms in <I>Pv-Cre;Shank2</I><SUP>fl/fl</SUP> mice, measured by electroencephalography, were normal, but susceptibility to pentylenetetrazole (PTZ)-induced seizures was decreased. These results suggest that <I>Shank2</I> deletion in PV-positive neurons leads to hyperactivity, enhanced self-grooming and suppressed brain excitation.</P>