Pt-AlGaN/GaN HEMT-based hydrogen gas sensors with and without SiNx post-passivation

tuan anh vuong,김형탁 한국전기전자학회 2019 전기전자학회논문지 Vol.23 No.3

GaN-based sensors have been widely investigated thanks to its potential in detecting the presence of hydrogen. In this study, we fabricated hydrogen gas sensors with AlGaN/GaN heterojunction and investigated how thesensing performance to be affected by SiN surface passivation. The gas sensor employed a high electron mobilitytransistors (HEMTs) with 30 nm platinum catalyst as a gate to detect the hydrogen presence. SiN layer wasdeposited by inductively-coupled chemical vapor deposition as post-passivation. The sensors with SiN passivationexhibited hydrogen sensing characteristics with various gas flow rates and concentrations of hydrogen in inertbackground gas at 200 oC similar to the ones without passivation. Aside from quick response time for bothsensors, there are differences in sensitivity and recovery time because of the existence of the passivation layer. The results also confirmed the dependence of sensing performance on gas flow rate and gas concentration.

SGTb regulates a surface localization of a guidance receptor BOC to promote neurite outgrowth

Vuong, Tuan Anh,Lee, Sang-Jin,Leem, Young-Eun,Lee, Jae-Rin,Bae, Gyu-Un,Kang, Jong-Sun Elsevier 2019 Cellular signalling Vol.55 No.-

<P><B>Abstract</B></P> <P>Neuritogenesis is a critical event for neuronal differentiation and neuronal circuitry formation during neuronal development and regeneration. Our previous study revealed a critical role of a guidance receptor BOC in a neuronal differentiation and neurite outgrowth. However, regulatory mechanisms for BOC signaling pathway remain largely unexplored. In the current study, we have identified Small glutamine-rich tetratricopeptide repeat (TPR)-containing b (SGTb) as a BOC interacting protein through yeast two-hybrid screening. Like BOC, SGTb is highly expressed in brain and P19 embryonal carcinoma (EC) cells differentiated into neuronal cells. BOC and SGTb proteins co-precipitate in mouse brain and differentiated P19 EC cells. Furthermore, BOC and SGTb co-localize in neurites and especially are concentrated at the tip of neurites in various neuronal cells. SGTb depletion attenuates neuronal differentiation of P19 cells through reduction of the surface level of BOC. Additionally, SGTb depletion causes BOC localization at neurite tip, coinciding with decreased p-JNK levels critical for actin cytoskeleton remodeling. The overexpression of SGTb or BOC restores JNK activation in BOC or SGTb-depleted cells, respectively. Finally, SGTb elevates the level of surface-resident BOC in BOC-depleted cells, restoring JNK activation. Taken together, our data suggest that SGTb interacts with BOC and regulates its surface level and consequent JNK activation, thereby promoting neuronal differentiation and neurite outgrowth.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The TPR-region of SGTb is critical for the interaction with the intracellular region of BOC. </LI> <LI> SGTb-BOC was colocalized at the tip of neurites during neuronal differentiation. </LI> <LI> SGTb restores neuronal differentiation and JNK activity in BOC-depleted cells. </LI> <LI> SGTb regulates BOC's localization at the tip of neurite and JNK activation. </LI> <LI> SGTb promotes neurogenesis and neurite outgrowth through BOC-mediated JNK activation. </LI> </UL> </P>

Pt-AlGaN/GaN HEMT-based hydrogen gas sensors with and without SiNx post-passivation

Vuong, Tuan Anh,Kim, Hyungtak Institute of Korean Electrical and Electronics Eng 2019 전기전자학회논문지 Vol.23 No.3

GaN-based sensors have been widely investigated thanks to its potential in detecting the presence of hydrogen. In this study, we fabricated hydrogen gas sensors with AlGaN/GaN heterojunction and investigated how the sensing performance to be affected by SiN surface passivation. The gas sensor employed a high electron mobility transistors (HEMTs) with 30 nm platinum catalyst as a gate to detect the hydrogen presence. SiN layer was deposited by inductively-coupled chemical vapor deposition as post-passivation. The sensors with SiN passivation exhibited hydrogen sensing characteristics with various gas flow rates and concentrations of hydrogen in inert background gas at $200^{\circ}C$ similar to the ones without passivation. Aside from quick response time for both sensors, there are differences in sensitivity and recovery time because of the existence of the passivation layer. The results also confirmed the dependence of sensing performance on gas flow rate and gas concentration.

Methylation determines the extracellular calcium sensitivity of the leak channel NALCN in hippocampal dentate granule cells

Seul-Yi Lee,Tuan Anh Vuong,Xianlan Wen,Hyeon-Ju Jeong,Hyun-Kyung So,Ilmin Kwon,Jong-Sun Kang,Hana Cho 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-

The sodium leak channel NALCN is a key player in establishing the resting membrane potential (RMP) in neurons andtransduces changes in extracellular Ca2+ concentration ([Ca2+]e) into increased neuronal excitability as thedownstream effector of calcium-sensing receptor (CaSR). Gain-of-function mutations in the human NALCN gene causeencephalopathy and severe intellectual disability. Thus, understanding the regulatory mechanisms of NALCN isimportant for both basic and translational research. This study reveals a novel mechanism for NALCN regulation byarginine methylation. Hippocampal dentate granule cells in protein arginine methyltransferase 7 (PRMT7)-deficientmice display a depolarization of the RMP, decreased threshold currents, and increased excitability compared to wildtypeneurons. Electrophysiological studies combined with molecular analysis indicate that enhanced NALCN activitiescontribute to hyperexcitability in PRMT7−/− neurons. PRMT7 depletion in HEK293T cells increases NALCN activity byshifting the dose-response curve of NALCN inhibition by [Ca2+]e without affecting NALCN protein levels. In vitromethylation studies show that PRMT7 methylates a highly conserved Arg1653 of the NALCN gene located in thecarboxy-terminal region that is implicated in CaSR-mediated regulation. A kinase-specific phosphorylation siteprediction program shows that the adjacent Ser1652 is a potential phosphorylation site. Consistently, our data fromsite-specific mutants and PKC inhibitors suggest that Arg1653 methylation might modulate Ser1652 phosphorylationmediated by CaSR/PKC-delta, leading to [Ca2+]e-mediated NALCN suppression. Collectively, these data suggest thatPRMT7 deficiency decreases NALCN methylation at Arg1653, which, in turn, decreases CaSR/PKC-mediated Ser1652phosphorylation, lifting NALCN inhibition, thereby enhancing neuronal excitability. Thus, PRMT7-mediated NALCNinhibition provides a potential target for the development of therapeutic tools for neurological diseases.

PRMT7 deficiency causes dysregulation of the HCN channels in the CA1 pyramidal cells and impairment of social behaviors

Seul-Yi Lee,Tuan Anh Vuong,Hyun-Kyung So,Hyun-Ji Kim,Yoo Bin Kim,Jong-Sun Kang,Ilmin Kwon,Hana Cho 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

HCN channels regulate excitability and rhythmicity in the hippocampal CA1 pyramidal cells. Perturbation in the HCN channel current (Ih) is associated with neuropsychiatric disorders, such as autism spectrum disorders. Recently, protein arginine methyltransferase 7 (PRMT7) was shown to be highly expressed in the hippocampus, including the CA1 region. However, the physiological function of PRMT7 in the CA1 neurons and the relationship to psychiatric disorders are unclear. Here we showed that PRMT7 knockout (KO) mice exhibit hyperactivity and deficits in social interaction. The firing frequency of the CA1 neurons in the PRMT7 KO mice was significantly higher than that in the wild-type (WT) mice. Compared with the WT CA1 neurons, the PRMT7 KO CA1 neurons showed a more hyperpolarized resting potential and a higher input resistance, which were occluded by the Ih-current inhibitor ZD7288; these findings were consistent with the decreased Ih and suggested the contribution of Ih-channel dysfunction to the PRMT7 KO phenotypes. The HCN1 protein level was decreased in the CA1 region of the PRMT7 KO mice in conjunction with a decrease in the expression of Shank3, which encodes a core scaffolding protein for HCN channel proteins. A brief application of the PRMT7 inhibitor DS437 did not reproduce the phenotype of the PRMT7 KO neurons, further indicating that PRMT7 regulates Ih by controlling the channel number rather than the open probability. Moreover, shRNA-mediated PRMT7 suppression reduced both the mRNA and protein levels of SHANK3, implying that PRMT7 deficiency might be responsible for the decrease in the HCN protein levels by altering Shank3 expression. These findings reveal a key role for PRMT7 in the regulation of HCN channel density in the CA1 pyramidal cells that may be amenable to pharmacological intervention for neuropsychiatric disorders.

Prmt7 Deficiency Causes Reduced Skeletal Muscle Oxidative Metabolism and Age-Related Obesity

Jeong, Hyeon-Ju,Lee, Hye-Jin,Vuong, Tuan Anh,Choi, Kyu-Sil,Choi, Dahee,Koo, Sung-Hoi,Cho, Sung Chun,Cho, Hana,Kang, Jong-Sun American Diabetes Association 2016 Diabetes Vol.65 No.7

<P>Maintenance of skeletal muscle function is critical for metabolic health and the disruption of which exacerbates many chronic diseases such as obesity and diabetes. Skeletal muscle responds to exercise or metabolic demands by a fiber-type switch regulated by signaling transcription networks that remains to be fully defined. Here, we report that protein arginine methyltransferase 7 (Prmt7) is a key regulator for skeletal muscle oxidative metabolism. Prmt7 is expressed at the highest levels in skeletal muscle and decreased in skeletal muscles with age or obesity. Prmt7(-/-) muscles exhibit decreased oxidative metabolism with decreased expression of genes involved in muscle oxidative metabolism, including PGC-1 alpha. Consistently, Prmt7(-/-) mice exhibited significantly reduced endurance exercise capacities. Furthermore, Prmt7(-/-) mice exhibit decreased energy expenditure, which might contribute to the exacerbated age-related obesity of Prmt7(-/-) mice. Similarly to Prmt7(-/-) muscles, Prmt7 depletion in myoblasts also reduces PGC-1 alpha expression and PGC-1 alpha-promoter driven reporter activities. Prmt7 regulates PGC-1 alpha expression through interaction with and activation of p38 mitogen-activated protein kinase (p38MAPK), which in turn activates ATF2, an upstream transcriptional activator for PGC-1 alpha. Taken together, Prmt7 is a novel regulator for muscle oxidative metabolism via activation of p38MAPK/ATF2/PGC-1 alpha.</P>

Research article Black ginseng activates Akt signaling, thereby enhancing myoblast differentiation and myotube growth

Lee, Soo-Yeon,Go, Ga-Yeon,Vuong, Tuan Anh,Kim, Jee Won,Lee, Sullim,Jo, Ayoung,An, Jun Min,Kim, Su-Nam,Seo, Dong-Wan,Kim, Jin-Seok,Kim, Yong Kee,Kang, Jong-Sun,Lee, Sang-Jin,Bae, Gyu-Un The Korean Society of Ginseng 2018 Journal of Ginseng Research Vol.42 No.1

Background: Black ginseng (BG) has greatly enhanced pharmacological activities relative to white or red ginseng. However, the effect and molecular mechanism of BG on muscle growth has not yet been examined. In this study, we investigated whether BG could regulate myoblast differentiation and myotube hypertrophy. Methods: BG-treated C2C12 myoblasts were differentiated, followed by immunoblotting for myogenic regulators, immunostaining for a muscle marker, myosin heavy chain or immunoprecipitation analysis for myogenic transcription factors. Results: BG treatment of C2C12 cells resulted in the activation of Akt, thereby enhancing hetero-dimerization of MyoD and E proteins, which in turn promoted muscle-specific gene expression and myoblast differentiation. BG-treated myoblasts formed larger multinucleated myotubes with increased diameter and thickness, accompanied by enhanced Akt/mTOR/p70S6K activation. Furthermore, the BG treatment of human rhabdomyosarcoma cells restored myogenic differentiation. Conclusion: BG enhances myoblast differentiation and myotube hypertrophy by activating Akt/mTOR/p70S6k axis. Thus, our study demonstrates that BG has promising potential to treat or prevent muscle loss related to aging or other pathological conditions, such as diabetes.

Inducible Prmt1 ablation in adult vascular smooth muscle leads to contractile dysfunction and aortic dissection

Pyun Jung-Hoon,Ahn Byeong-Yun,Vuong Tuan Anh,Kim Su Woo,조윤주,Jeon Jaehyung,Baek Seung Ho,Kim Jaewon,Park Sungsu,배규운,Choi Jun-Hyuk,Kim Jae-Ryong,Ryu Dongryeol,Lee Sang-Jin,강종순 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-

Vascular smooth muscle cells (VSMCs) have remarkable plasticity in response to diverse environmental cues. Although these cells are versatile, chronic stress can trigger VSMC dysfunction, which ultimately leads to vascular diseases such as aortic aneurysm and atherosclerosis. Protein arginine methyltransferase 1 (Prmt1) is a major enzyme catalyzing asymmetric arginine dimethylation of proteins that are sources of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase. Although a potential role of Prmt1 in vascular pathogenesis has been proposed, its role in vascular function has yet to be clarified. Here, we investigated the role and underlying mechanism of Prmt1 in vascular smooth muscle contractility and function. The expression of PRMT1 and contractile-related genes was significantly decreased in the aortas of elderly humans and patients with aortic aneurysms. Mice with VSMC-specific Prmt1 ablation (smKO) exhibited partial lethality, low blood pressure and aortic dilation. The Prmt1-ablated aortas showed aortic dissection with elastic fiber degeneration and cell death. Ex vivo and in vitro analyses indicated that Prmt1 ablation significantly decreased the contractility of the aorta and traction forces of VSMCs. Prmt1 ablation downregulated the expression of contractile genes such as myocardin while upregulating the expression of synthetic genes, thus causing the contractile to synthetic phenotypic switch of VSMCs. In addition, mechanistic studies demonstrated that Prmt1 directly regulates myocardin gene activation by modulating epigenetic histone modifications in the myocardin promoter region. Thus, our study demonstrates that VSMC Prmt1 is essential for vascular homeostasis and that its ablation causes aortic dilation/dissection through impaired myocardin expression.

TGF-β-activated Kinase 1 (TAK1) and Apoptosis Signal-regulating Kinase 1 (ASK1) Interact with the Promyogenic Receptor Cdo to Promote Myogenic Differentiation via Activation of p38MAPK Pathway

Tran, Phong,Ho, Seok-Man,Kim, Bok-Geon,Vuong, Tuan Anh,Leem, Young-Eun,Bae, Gyu-Un,Kang, Jong-Sun American Society for Biochemistry and Molecular Bi 2012 The Journal of biological chemistry Vol.287 No.15

<P>p38MAPK plays an essential role in the transition of myoblasts to differentiated myotubes through the activation of MyoD family transcription factors. A promyogenic cell surface molecule, Cdo, promotes myogenic differentiation mainly through activation of the p38MAPK pathway. Two MAP3Ks, TAK1 and ASK1, can activate p38MAPK via MKK6 in various cell systems. Moreover TAK1 has been shown to promote myogenic differentiation via p38MAPK activation. In this study, we hypothesized that TAK1 and ASK1 might function as MAP3Ks in Cdo-mediated p38MAPK activation during myoblast differentiation. Both ASK1 and TAK1 were expressed in myoblasts and interacted with the cytoplasmic tail of Cdo and a scaffold protein, JLP. The depletion of TAK1 or ASK1 in C2C12 cells decreased myoblast differentiation, whereas overexpression of TAK1 or ASK1 in C2C12 cells enhanced myotube formation. In agreement with this, overexpression of ASK1 or TAK1 resulted in enhanced p38MAPK activation, and their knockdown inhibited p38MAPK in C2C12 cells. Overexpression of TAK1 or ASK1 in <I>Cdo</I><SUP>−/−</SUP> myoblasts and Cdo-depleted C2C12 cells restored p38MAPK activation as well as myotube formation. Furthermore, ASK1 and TAK1 compensated for each other in p38MAPK activation and myoblast differentiation. Taken together, these findings suggest that ASK1 and TAK1 function as MAP3Ks in Cdo-mediated p38MAPK activation to promote myogenic differentiation.</P>

Cultural Factors Affecting Tendency of Ethical Decision-Making by Accounting Students: An Empirical Study in Vietnam

Nga Thanh DOAN,Trang Thu TA,Ha Thi Thanh CHU,Anh Thi Quynh LE,May Thi LE,Tuan Hoang PHAM,Thao Thu VUONG 한국유통과학회 2022 The Journal of Asian Finance, Economics and Busine Vol.9 No.2

The purpose of this study is to look at the precise direction and magnitude of cultural elements such as education, gender, power distance, and risk-taking proclivity on ethical decision-making. Data was collected from 194 interviewees in three groups: general business students, accounting major students, and professional auditors in Vietnam. The path analysis is used to test the impact of cultural factors on ethical awareness, ethical judgment, and ethical intention in different dubious scenarios at the personal level as independent variables, intermediate variables, and moderating variables. The metric is the percentage of respondents who believe a particular behavior is unethical based on a set of ethical principles. The researchers used SPSS AMOS software to conduct a confirmatory factor survey to evaluate the convergent and discriminant validity of latent variables. The results show differences between the two groups of students and professionals on these measures, suggesting that all of the four factors have an effect on ethical decision-making. Based on research results, some recommendations are proposed related to the four factors to improve the ethics of future generations of auditors in Vietnam. This study also contributes to the theory of culture in particular and cultural interference in general in the field of accounting-auditing in Vietnam in the process of international integration.