• Microbiology and Biotechnology Letters
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• v.19 no.1
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• pp.37-44
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• 1991

- I aimed to isolate trans-acting factors involved in the basal expression level of eukaryotic genes. One of the yeast histidine biosynthetic gene, HIS5 was taken as a model for this study. HIS5 gene has a substantial basal level in amino acid rich medium and is derepressed if starved for any single amino acid. The derepression is mediated by cis-acting DNA sequences 5'-TGACTC-3' found in 5' non-transcribed region of the gene and trans-acting factors including GCN4 as positive factor and its negative factor GCDI 7, and GCNZ as a negative factor of GCD17. I first investigated the role of these trans-acting factors in HIS5 basal expression level by using HIS5-pH05 fusion in which expression of pH05 gene encoding inorganic phosphate-repressible acid phosphatase (APase) is regulated by HIS5 promoter. Strain with gcn2 or gcn4 mutation showed 3 to 4 fold lower APase activity than wild type. The level of APase activity was similar in gcn2 and gcn4 mutants. Trans-acting factors involved in basal level were identified by isolating 14 mutants showing increased expression of HISSPH05 fusion from gcn4 background. All the mutants carry a single nuclear recessive mutation and fall into four complementation groups, designated as bell (basal expression level), be12, be23 and be14.

• Biomedical Science Letters
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• v.19 no.3
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• pp.266-269
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• 2013

Hox genes encode transcription factors important for anterior-posterior body patterning at early stages of embryonic development. However, the precise mechanisms by which signal pathways are stimulated to regulate Hox gene expression are not clear. In the previous study, protein kinase B alpha (Akt1) has been identified as a putative upstream regulator of Hox genes, and Akt1 has shown to regulate Gcn5, a prototypical histone acetyltransferase (HAT), in a negative way in mouse embryonic fibroblast (MEF) cells. Since the activity of HAT such as the CBP/p300, and PCAF (a Gcn5 homolog), was down-regulated by Akt through a phosphorylation at the Akt consensus substrate motif (RXRXXS/T), the amino acid sequence of Gcn5 protein was analyzed. Mouse Gcn5 contains an Akt consensus substrate motif as RQRSQS sequence while human Gcn5 does not have it. In order to see whether Akt1 directly binds to Gcn5, immunoprecipitation with anti-Akt1 antibody was carried out in wild-type (WT) mouse embryonic fibroblast (MEF) cells, and then western blot analysis was performed with anti-Akt1 and anti-Gcn5 antibodies. Gcn5 protein was detected in the Akt1 immunoprecipitated samples of MEFs. This result demonstrates that Akt1 directly binds to Gcn5, which might have contributed the down regulation of the 5' Hoxc gene expressions in wild type MEF cells.

• Biomedical Science Letters
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• v.18 no.2
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• pp.165-168
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• 2012

Hox proteins containing DNA-binding homedomain act as transcription factors important for anteroposterior body patterning during vertebrate embryogenesis. However, the precise mechanisms by which signal pathways are transduced to regulate the Hox gene expression are not clear. In the course of an attempt to isolate an upstream regulatory factor(s) controlling Hox genes, protein kinase B alpha (Akt1) has been identified as a putative regulator of Hox genes through in silico analysis (GEO profile). In the Gene Expression Omnibus (GEO) dataset GDS1784 at the NCBI (National Center for Biotechnology Information) site, Hox genes were differentially expressed depending on the presence or absence of Akt1. Since it was not well known how Akt1 regulates the specific Hox genes, whose transcription was reported to be regulated by epigenetic modifications such as histone acetylation, methylation etc., the expression of Gcn5, a histone acetyltransferase (HAT), was analyzed in wild type (WT) as well as in $Akt1^{-/-}$ mouse embryonic fibroblast (MEF) cells. RT-PCR analysis revealed that the amount of Gcn5 mRNA was similar in both WT and $Akt1^{-/-}$ MEFs. However, the protein level of Gcn5 was significantly increased in $Akt1^{-/-}$ MEF cells. The half life of Gcn5 was 1 hour in wild type whereas 8 hours in $Akt1^{-/-}$ MEF. These data all together, indicate that Gcn5 is post-transcriptionally down-regulated and the protein stability is negatively regulated by Akt1 in MEF cells.

• The Journal of the Korea institute of electronic communication sciences
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• v.17 no.5
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• pp.801-808
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• 2022

Research on how to embed knowledge in large-scale Linked Data and apply neural network models for entity matching is relatively scarce. The most fundamental problem with this is that different labels lead to lexical heterogeneity. In this paper, we propose an extended GCN (Graph Convolutional Network) model that combines re-align structure to solve this lexical heterogeneity problem. The proposed model improved the performance by 53% and 40%, respectively, compared to the existing embedded-based MTransE and BootEA models, and improved the performance by 5.1% compared to the GCN-based RDGCN model.

• KSII Transactions on Internet and Information Systems (TIIS)
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• v.14 no.5
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• pp.1909-1928
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• 2020

Predicting human mobility has always been an important task in Location-based Social Network. Previous efforts fail to capture spatial dependence effectively, mainly reflected in weakening the location topology information. In this paper, we propose a neural network-based method which can capture spatial-temporal dependence to predict the next location of a person. Specifically, we involve a graph convolutional network (GCN) based on a seq2seq framework to capture the location topology information and temporal dependence, respectively. The encoder of the seq2seq framework first generates the hidden state and cell state of the historical trajectories. The GCN is then used to generate graph embeddings of the location topology graph. Finally, we predict future trajectories by aggregated temporal dependence and graph embeddings in the decoder. For evaluation, we leverage two real-world datasets, Foursquare and Gowalla. The experimental results demonstrate that our model has a better performance than the compared models.

• Molecules and Cells
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• v.38 no.12
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• pp.1037-1043
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• 2015

The TAZ activator 2-butyl-5-methyl-6-(pyridine-3-yl)-3-[2'-(1H-tetrazole-5-yl)-biphenyl-4-ylmethyl]-3H-imidazo[4,5-b]pyridine] (TM-25659) inhibits adipocyte differentiation by interacting with peroxisome proliferator-activated receptor gamma. 1 TM-25659 was previously shown to decrease weight gain in a high fat (HF) diet-induced obesity (DIO) mouse model. However, the fundamental mechanisms underlying the effects of TM-25659 remain unknown. Therefore, we investigated the effects of TM-25659 on skeletal muscle functions in C2 myotubes and C57BL/6J mice. We studied the molecular mechanisms underlying the contribution of TM-25659 to palmitate (PA)-induced insulin resistance in C2 myotubes. TM-25659 improved PA-induced insulin resistance and inflammation in C2 myotubes. In addition, TM-25659 increased FGF21 mRNA expression, protein levels, and FGF21 secretion in C2 myotubes via activation of GCN2 pathways (GCN2-$phosphoelF2{\alpha}$-ATF4 and FGF21). This beneficial effect of TM-25659 was diminished by FGF21 siRNA. C57BL/6J mice were fed a HF diet for 30 weeks. The HF-diet group was randomly divided into two groups for the next 14 days: the HF-diet and HF-diet + TM-25659 groups. The HF diet + TM-25659-treated mice showed improvements in their fasting blood glucose levels, insulin sensitivity, insulin-stimulated Akt phosphorylation, and inflammation, but neither body weight nor food intake was affected. The HF diet + TM-25659-treated mice also exhibited increased expression of both FGF21 mRNA and protein. These data indicate that TM-25659 may be beneficial for treating insulin resistance by inducing FGF21 in models of PA-induced insulin resistance and HF diet-induced insulin resistance.

• Smart Media Journal
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• v.12 no.11
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• pp.113-124
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• 2023

With the advent of 5G and B5G (Beyond 5G) networks, network virtualization technology that can overcome the limitations of existing networks is attracting attention. The purpose of network virtualization is to provide solutions for efficient network resource utilization and various services. Existing heuristic-based VNE (Virtual Network Embedding) techniques have been studied, but the flexibility is limited. Therefore, in this paper, we propose a GNN-based network slicing classification scheme to meet various service requirements and a RL-based VNE scheme for optimal resource allocation. The proposed method performs optimal VNE using an Actor-Critic network. Finally, to evaluate the performance of the proposed technique, we compare it with Node Rank, MCST-VNE, and GCN-VNE techniques. Through performance analysis, it was shown that the GNN and RL-based VNE techniques are better than the existing techniques in terms of acceptance rate and resource efficiency.

• Asian-Australasian Journal of Animal Sciences
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• v.32 no.1
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• pp.110-117
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• 2019

Objective: An experiment was conducted to evaluate the effects of dietary glutamine (Gln) and arginine (Arg) supplementation on performance, intestinal morphology and ascites mortality in broilers. Methods: A total of 675 day old chicks were randomly allocated to 9 experimental groups in a $3{\times}3$ factorial arrangement based on a completely randomized design with 5 replicates of 15 chicks. Three levels of dietary Gln (0%, 0.5%, and 1%) and Arg (100%, 130%, and 160% of Ross recommendation) supplementation were used in ascites inducing condition ($15^{\circ}C{\pm}1^{\circ}C$) from 7 to 42 days of age. Results: Dietary supplementation of Gln increased body weight gain during grower, finisher and total periods (p<0.05) and increased feed intake during total period. Ascites mortality was decreased by Gln supplementation (p<0.05). Gln supplementation increased the villus height (VH) and crypt depth (CD) in duodenum and jejunum (p<0.05). Arg supplementation decreased CD in duodenum and jejunum, and increased ileum villus width (VW) and also VH/CD ratio in duodenum and jejunum (p<0.05). Both Gln and Arg increased the goblet cell number (GCN) in duodenum whereas Gln supplementation decreased GCN in jejunum and ileum (p<0.05). The $Gln{\times}Arg$ interaction were observed for right ventricle (RV)/total ventricular (TV) ratio, VH, VW, CD, VH/CD. Conclusion: It was concluded that dietary 0.5% Gln alone or along with 130% Arg of Ross requirement, improve the intestinal morphology and performance and hence decrease the ascites mortality in broiler chickens with cold induced ascites.

• Molecules and Cells
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• v.39 no.5
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• pp.410-417
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• 2016

During the lactation cycle of the bovine mammary gland, autophagy is induced in bovine mammary epithelial cells (BMECs) as a cellular homeostasis and survival mechanism. Interferon gamma ($IFN-{\gamma}$) is an important antiproliferative and apoptogenic factor that has been shown to induce autophagy in multiple cell lines in vitro. However, it remains unclear whether $IFN-{\gamma}$ can induce autophagy and whether autophagy affects milk synthesis in BMECs. To understand whether $IFN-{\gamma}$ affects milk synthesis, we isolated and purified primary BMECs and investigated the effect of $IFN-{\gamma}$ on milk synthesis in primary BMECs in vitro. The results showed that $IFN-{\gamma}$ significantly inhibits milk synthesis and that autophagy was clearly induced in primary BMECs in vitro within 24 h. Interestingly, autophagy was observed following $IFN-{\gamma}$ treatment, and the inhibition of autophagy can improve milk protein and milk fat synthesis. Conversely, upregulation of autophagy decreased milk synthesis. Furthermore, mechanistic analysis confirmed that $IFN-{\gamma}$ mediated autophagy by depleting arginine and inhibiting the general control nonderepressible-2 kinase (GCN2)/eukaryotic initiation factor $2{\alpha}$ ($eIF2{\alpha}$) signaling pathway in BMECs. Then, it was found that arginine supplementation could attenuate $IFN-{\gamma}$-induced autophagy and recover milk synthesis to some extent. These findings may not only provide a novel measure for preventing the $IFN-{\gamma}$-induced decrease in milk quality but also a useful therapeutic approach for $IFN-{\gamma}$-associated breast diseases in other animals and humans.

• Korean Journal of Plant Resources
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• v.22 no.3
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• pp.203-208
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• 2009

Lunasin is a unique 43-amino acid peptide which has shown a chemopreventive in mammalian cells and in a skin cancer mouse model. In search for new sources of lunasin and the role of cereals in cancer prevention, we report here the properties of lunasin purified from millet. Stability of millet lunasin was measured by in vitro digestibility assay using pepsin and pancreatin. Inhibition of HAT (histone acetyltransferase) and nuclear localization in mammalian cells were used to measure lunasin bioactivity as the cancer chemopreventive agent. Lunasin present in millet crude protein was stable to pepsin and pancreatin in in vitro digestion and inhibited the activities of HATs. When added exogenously, lunasin purified from millet internalized in the nuclei of mouse fibroblast cells. On the base of this result, we conclude that lunasin in millet is bioactive and consumption of millet may play an important role on cancer prevention in millet-consuming populations.