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Excitatory neuron–specific SHP2-ERK signaling network regulates synaptic plasticity and memory
Ryu, Hyun-Hee,Kim, TaeHyun,Kim, Jung-Woong,Kang, Minkyung,Park, Pojeong,Kim, Yong Gyu,Kim, Hyopil,Ha, Jiyeon,Choi, Ja Eun,Lee, Jisu,Lim, Chae-Seok,Kim, Chul-Hong,Kim, Sang Jeong,Silva, Alcino J.,Kaang AAAS 2019 Science signaling Vol.12 No.571
<P><B>Cell type–specific RASopathy</B></P><P>The neurodevelopmental disorder Noonan syndrome is often caused by activating mutations in the phosphatase SHP2 that enhance RAS signaling. However, SHP2 is present in multiple neuron types as well as glia; thus, where the mutant protein has its pathological effects is unclear. Ryu <I>et al.</I> examined one NS-associated SHP2 mutation in isolated cell types from mice and determined that its presence in only excitatory neurons resulted in electrophysiological and cognitive effects. This was because certain adaptor proteins that interact with SHP2 to mediate RAS signaling are abundant in excitatory but not inhibitory neurons. These findings reveal that cell type–specific variations within the RAS signaling network underlie the phenotypes of NS and possibly other “RASopathies”.</P><P>Mutations in RAS signaling pathway components cause diverse neurodevelopmental disorders, collectively called RASopathies. Previous studies have suggested that dysregulation in RAS–extracellular signal–regulated kinase (ERK) activation is restricted to distinct cell types in different RASopathies. Some cases of Noonan syndrome (NS) are associated with gain-of-function mutations in the phosphatase SHP2 (encoded by <I>PTPN11</I>); however, SHP2 is abundant in multiple cell types, so it is unclear which cell type(s) contribute to NS phenotypes. Here, we found that expressing the NS-associated mutant SHP2<SUP>D61G</SUP> in excitatory, but not inhibitory, hippocampal neurons increased ERK signaling and impaired both long-term potentiation (LTP) and spatial memory in mice, although endogenous SHP2 was expressed in both neuronal types. Transcriptomic analyses revealed that the genes encoding SHP2-interacting proteins that are critical for ERK activation, such as GAB1 and GRB2, were enriched in excitatory neurons. Accordingly, expressing a dominant-negative mutant of GAB1, which reduced its interaction with SHP2<SUP>D61G</SUP>, selectively in excitatory neurons, reversed SHP2<SUP>D61G</SUP>-mediated deficits. Moreover, ectopic expression of GAB1 and GRB2 together with SHP2<SUP>D61G</SUP> in inhibitory neurons resulted in ERK activation. These results demonstrate that RAS-ERK signaling networks are notably different between excitatory and inhibitory neurons, accounting for the cell type–specific pathophysiology of NS and perhaps other RASopathies.</P>
Rediscovery of antimicrobial peptides as therapeutic agents
Minkyung Ryu,Jaeyeong Park,Ji-Hyun Yeom,주민주,Kangseok Lee 한국미생물학회 2021 The journal of microbiology Vol.59 No.2
In recent years, the occurrence of antibiotic-resistant pathogens is increasing rapidly. There is growing concern as the development of antibiotics is slower than the increase in the resistance of pathogenic bacteria. Antimicrobial peptides (AMPs) are promising alternatives to antibiotics. Despite their name, which implies their antimicrobial activity, AMPs have recently been rediscovered as compounds having antifungal, antiviral, anticancer, antioxidant, and insecticidal effects. Moreover, many AMPs are relatively safe from toxic side effects and the generation of resistant microorganisms due to their target specificity and complexity of the mechanisms underlying their action. In this review, we summarize the history, classification, and mechanisms of action of AMPs, and provide descriptions of AMPs undergoing clinical trials. We also discuss the obstacles associated with the development of AMPs as therapeutic agents and recent strategies formulated to circumvent these obstacles.
Ryu Minkyung,Kim Minsu,Jung Hyun Young,Kim Cho Hyun,조철훈 아세아·태평양축산학회 2023 Animal Bioscience Vol.36 No.2
Objective: Inhibiting the p38 mitogen-activated protein kinase (MAPK) signaling pathway delays differentiation and increases proliferation of muscle stem cells in most species. Here, we aimed to investigate the effect of p38 inhibitor (p38i) treatment on the proliferation and differentiation of chicken muscle stem cells. Methods: Chicken muscle stem cells were collected from the muscle tissues of Hy-line Brown chicken embryos at embryonic day 18, then isolated by the preplating method. Cells were cultured for 4 days in growth medium supplemented with dimethyl sulfoxide or 1, 10, 20 μM of p38i, then subcultured for up to 4 passages. Differentiation was induced for 3 days with differentiation medium. Each treatment was replicated 3 times. Results: The proliferation and mRNA expression of paired box 7 gene and myogenic factor 5 gene, as well as the mRNA expression of myogenic differentiation marker gene myogenin were significantly higher in p38i-treated cultures than in control (p<0.05), but immunofluorescence staining and mRNA expression of myosin heavy chain (MHC) were not significantly different between the two groups. Oil red O staining of accumulated lipid droplets in differentiated cell cultures revealed a higher lipid density in p38i-treated cultures than in control; however, the expression of the adipogenic marker gene peroxisome proliferator activated receptor gamma was not significantly different between the two groups. Conclusion: p38 inhibition in chicken muscle stem cells improves cell proliferation, but the effects on myogenic differentiation and lipid accumulation require additional analysis. Further studies are needed on the chicken p38-MAPK pathway to understand the muscle and fat development mechanism.
대류·복사 연성시뮬레이션을 통한 옥외 온열환경 평가 기법
류민경(Minkyung RYU),임종연(Jong-Yeon Lim),황효근(Hyo-Keun Hwang),송두삼(Doo-Sam Song) 대한설비공학회 2009 대한설비공학회 학술발표대회논문집 Vol.2009 No.-
Deterioration of the outdoor thermal environment in urban areas such as heat island has become worse due to urbanization and overpopulation, etc. In this study, a new method which is coupled simulation of convection and radiation to evaluate outdoor thermal environment in urban area will be proposed. Because the solar radiation affects on outdoor thermal environment massively, therefore the radiation calculation is very important in outdoor thermal environment prediction. The coupled simulation proposed in this study can assess the outdoor thermal environment with accurate.
( Woo Kyung Ryu ),( Jung Soo Kim ),( Mi Hwa Park ),( Minkyung Lee ),( Hyun-jung Kim ),( Jeong-seon Ryu ),( Jun Hyeok Lim ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Background A heterogenous radiological response is frequently observed in cancer patients and could reflect tumor heterogeneity. We investigated the prognostic impact of heterogeneous radiological responses in patients with advanced non-small cell lung cancer (NSCLC) who received platinum-based chemotherapy. Methods The treatment response according to RECIST 1.1 (Response Evaluation Criteria in Solid Tumors) criteria were evaluated in 212 patients with advanced NSCLC who received platinum-based chemotherapy. Patients with partial response (PR) or stable disease (SD) were classified into “PR homo,” “PR hetero,” “SD homo,” and “SD hetero” by the presence of a heterogenous radiological response, and survival was compared between groups. We also compared survival based on the presence of metabolic responses in lesions with heterogeneous radiological responses. Results Fifty-two patients (24.5%) were classified as PR, 112 patients (52.8%) as SD, and 48 patients (22.7%) as progressive disease (PD). There was no significant difference in progression-free survival (PFS) and overall survival (OS) between the PR homo and PR hetero groups. The SD homo group had a longer PFS and OS than the SD hetero group (Figure 1). In the SD hetero group, patients with increased maximum standardized uptake value (SUVmax) in lesions with heterogenous radiological responses had a shorter PFS than those with a stable SUVmax (Figure 2). Conclusions The presence of lesions with radiological heterogeneity was associated with disease progression and poor prognosis in the SD group. Patients with heterogeneous radiological responses therefore required careful monitoring.
Ryu, Jihye,Kang, Minkyung,Lee, Mi-Sook,Kim, Hye-Jin,Nam, Seo Hee,Song, Haeng Eun,Lee, Doohyung,Lee, Jung Weon American Society for Microbiology 2014 Molecular and cellular biology Vol.34 No.16
<P>TM4SF5 overexpressed in hepatocellular carcinoma activates focal adhesion kinase (FAK) during tumor cell migration. However, it remains unknown how TM4SF5 in hepatocellular carcinoma cells compromises with immune actions initiated by extracellular cytokines. Normal and cancerous hepatocytes with or without TM4SF5 expression were analyzed for the effects of cytokine signaling activity on TM4SF5/FAK signaling and metastatic potential. We found that interleukin-6 (IL-6) was differentially expressed in hepatocytes depending on cancerous malignancy and TM4SF5 expression. IL-6 treatment activated FAK and STAT3 and enhanced focal adhesion (FA) formation in TM4SF5-null cells, but it decreased TM4SF5-dependent FAK activity and FA formation in SNU761-TM4SF5 cells. STAT3 suppression abolished the IL-6-mediated effects in normal Chang cells, but it did not recover the TM4SF5-dependent FAK activity that was inhibited by IL-6 treatment in cancerous SNU761-TM4SF5 cells. In addition, modulation of FAK activity did not change the IL-6-mediated STAT3 activity in either the Chang or SNU761 cell system. TM4SF5 expression in SNU761 cells caused invasive extracellular matrix degradation negatively depending on IL-6/IL-6 receptor (IL-6R) signaling. Thus, it is likely that hepatic cancer cells adopt TM4SF5-dependent FAK activation and metastatic potential by lowering IL-6 expression and avoiding its immunological action through the IL-6-STAT3 pathway.</P>