• Title/Summary/Keyword: Atf3

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A New Calibration Method for the Characterization of Microwave Devices (마이크로파 소자 특성화를 위한 새로운 보정 방법)

  • 신헌철;유영길;정의붕;이종악
    • The Proceeding of the Korean Institute of Electromagnetic Engineering and Science
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    • v.2 no.3
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    • pp.10-16
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    • 1991
  • The error networks due to the measuring systems and the test fixture must be previously calibrated in order to characterize the microwave devices. In this paper, it is presented a new method to characterize the error networks in which only two different microstrip lines are used for the calibration. Once each length of two calibrat- ing microstrip lines is accurately defined, the calibrated data can be easily obtained without acknowledgement for the propagation constant. The end effect is not considered when fabricated the microstrip lines used to calibration. The ATF13736 GaAs MESFET is characterized by means of the calibrating procedure with this method. The range of measuring frequency is 2 to 18 GHz, and the bias voltage and current are $V_{DS}$ =2.5V, $I_{DS}$ =20mA, respectively. Compared the calibrated data with data sheet, it is showed that the magnitude is nearly agreed with each other and the phase is deviated by 0.1 to 12 degrees in lower frequencies.

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Investigation on effect of surface properties on droplet impact cooling of cladding surfaces

  • Wang, Zefeng;Qu, Wenhai;Xiong, Jinbiao;Zhong, Mingjun;Yang, Yanhua
    • Nuclear Engineering and Technology
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    • v.52 no.3
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    • pp.508-519
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    • 2020
  • During transients or accidents, the reactor core is uncovered, and droplets entrained above the quench front collides with the uncovered fuel rod surface. Droplet impact cooling can reduce the peak cladding temperature. Besides zirconium-based cladding, versatile accidental tolerant fuel (ATF) claddings, including FeCrAl, have been proposed to increase the accident coping time. In order to investigate the effect of surface properties on droplet impact cooling of cladding surfaces, the droplet impact phenomena are photographed on the FeCrAl and zircaloy-4 (Zr-4) surfaces under different conditions. On the oxidized FeCrAl surface, the Leidenfrost phenomenon is not observed even when the surface temperature is as high as 550 ℃ with We > 30. Comparison of the impact behaviors observed on different materials shows that nucleate and transition boiling is more intensive on surfaces with larger thermal conductivity. The Leidenfrost point temperature (LPT) decreases with the solid thermal effusivity (${\sqrt{k{\rho}C_p}}$). However, the CHF temperature is relatively insensitive to the surface oxidation and Weber number. Droplet spreading diameter is analyzed quantitatively in the film boiling stage. Based on the energy balance a correlation is proposed for droplet maximum spreading factor. A mechanistic model is also developed for the LPT based on homogeneous nucleation theory.

Linkage and association scan for tanning ability in an isolated Mongolian population

  • Paik, Seung-Hwan;Kim, Hyun-Jin;Lee, Seung-Bok;Im, Sun-Wha;Ju, Young-Seok;Yeon, Je-Ho;Jo, Seong-Jin;Eun, Hee-Chul;Seo, Jeong-Sun;Kim, Jong-Il;Kwon, Oh-Sang
    • BMB Reports
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    • v.44 no.11
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    • pp.741-746
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    • 2011
  • Tanning ability is important, because it represents the ability of the skin to protect itself against ultraviolet (UV) radiation. Here, we sought to determine genetic regions associated with tanning ability. Skin pigmentation was measured at the outer forearm and buttock areas to represent facultative and constitutive skin color, respectively. In our study population consisting of isolated Mongolian subjects, with common histories of environmental UV exposure during their nomadic life, facultative skin color adjusted by constitutive skin color was used to indicate tanning ability. Through linkage analysis and family-based association tests of 345 Mongolian subjects, we identified 2 potential linkage regions regulating tanning ability on 5q35.3 and 12q13.2, having 6 and 7 significant single nucleotide polymorphisms (SNPs), respectively. Those significant SNPs were located in or adjacent to potential candidate genes related to tanning ability: GRM6, ATF1, WNT1, and SILV/Pmel17.

Induction of Cyclin D1 Proteasomal Degradation by Branch Extracts from Abeliophyllum distichum Nakai in Human Colorectal Cancer Cells

  • Park, Gwang Hun;Park, Jae Ho;Jeong, Jin Boo
    • Korean Journal of Plant Resources
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    • v.28 no.6
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    • pp.682-689
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    • 2015
  • Abeliophyllum distichum Nakai (A. distichum) has been reported to exert the inhibitory effect on angiotensin converting enzyme and aldose reductase. Recently, our group found that branch extracts of A. distichum (EAFAD-B) induce apoptosis through ATF3 activation in human colon cancer cells. However, anti-cancer reagents exert their activity through the regulation of various molecular targets. Therefore, the elucidation of potential mechanisms of EAFAD-B for anti-cancer activity may be necessary. To elucidate the potential mechanism of EAFAD-B for anti-cancer activity, we evaluated the regulation of cyclin D1 in human colon cancer cells. EAFAD-B decreased cellular accumulation of cyclin D1 protein. However, cyclin D1 mRNA was not changed by EAFAD-B. Inhibition of proteasomal degradation by MG132 attenuated EAFAD-B-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with EAFAD-B. In addition, EAFAD-B induced cyclin D1 phosphorylation at threonine-286 and the point mutation of threonine-286 to alanine attenuated EAFAD-B-mediated cyclin D1 proteasomal degradation. Inhibitions of both ERK1/2 by PD98059 and NF-κB by a selective inhibitor, BAY 11-7082 suppressed cyclin D1 downregulation by EAFAD-B. From these results, we suggest that EAFAD-B-mediated cyclin D1 downregulation may result from proteasomal degradation through its threonine-286 phosphorylation via ERK1/2-dependent NF-κB activation. The current study provides new mechanistic link between EAFAD-B and anti-cancer activity in human colon cancer cells.

G protein-coupled estrogen receptor-1 agonist induces chemotherapeutic effect via ER stress signaling in gastric cancer

  • Lee, Seon-Jin;Kim, Tae Woo;Park, Gyeong Lim;Hwang, Yo Sep;Cho, Hee Jun;Kim, Jong-Tae;Lee, Hee Gu
    • BMB Reports
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    • v.52 no.11
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    • pp.647-652
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    • 2019
  • G protein-coupled estrogen receptor (GPER) is known to play an important role in hormone-associated cancers. G-1, a novel synthetic GPER agonist, has been reported to exhibit anti-carcinogenic properties. However, the chemotherapeutic mechanism of GPER is yet unclear. Here, we evaluated GPER expression in human gastric cancer tissues and cells. We found that G-1 treatment attenuates GPER expression in gastric cancer. GPER expression increased G-1-induced antitumor effects in mouse xenograft model. We analyzed the effects of knockdown/overexpression of GPER on G-1-induced cell death in cancer cells. Increased GPER expression in human gastric cancer cells increased G-1-induced cell death via increased levels of cleaved caspase-3, -9, and cleaved poly ADP-ribose polymerase. Interestingly, during G-1-induced cell death, GPER mRNA and protein expression was attenuated and associated with ER stress-induced expression of PERK, ATF-4, GRP-78, and CHOP. Furthermore, PERK-dependent induction of ER stress activation increased G-1-induced cell death, whereas PERK silencing decreased cell death and increased drug sensitivity. Taken together, the data suggest that the induction of ER stress via GPER expression may increase G-1-induced cell death in gastric cancer cells. These results may contribute to a new paradigm shift in gastric cancer therapy.

Endoplasmic Reticulum Stress Activates Hepatic Macrophages through PERK-hnRNPA1 Signaling

  • Ari Kwon;Yun Seok Kim;Jiyoon Kim;Ja Hyun Koo
    • Biomolecules & Therapeutics
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    • v.32 no.3
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    • pp.341-348
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    • 2024
  • Endoplasmic reticulum (ER) stress plays a crucial role in liver diseases, affecting various types of hepatic cells. While studies have focused on the link between ER stress and hepatocytes as well as hepatic stellate cells (HSCs), the precise involvement of hepatic macrophages in ER stress-induced liver injury remains poorly understood. Here, we examined the effects of ER stress on hepatic macrophages and their role in liver injury. Acute ER stress led to the accumulation and activation of hepatic macrophages, which preceded hepatocyte apoptosis. Notably, macrophage depletion mitigated liver injury induced by ER stress, underscoring their detrimental role. Mechanistic studies revealed that ER stress stimulates macrophages predominantly via the PERK signaling pathway, regardless of its canonical substrate ATF4. hnRNPA1 has been identified as a crucial mediator of PERK-driven macrophage activation, as the overexpression of hnRNPA1 effectively reduced ER stress and suppressed pro-inflammatory activation. We observed that hnRNPA1 interacts with mRNAs that encode UPR-related proteins, indicating its role in the regulation of ER stress response in macrophages. These findings illuminate the cell type-specific responses to ER stress and the significance of hepatic macrophages in ER stress-induced liver injury. Collectively, the PERK-hnRNPA1 axis has been discovered as a molecular mechanism for macrophage activation, presenting prospective therapeutic targets for inflammatory hepatic diseases such as acute liver injury.

Expression of Fra1 and Fra2 Genes are regulated by Estrogen in the Mouse Uterus (생쥐자궁에서 에스트로겐에 의해 조절되는 Fra1과 Fra2 유전자의 발현양상)

  • Lee, Ji-Yoon;Hong, Seok-Ho;Nah, Hee-Young;Kim, Sung-Hoon;Chae, Hee-Dong;Kim, Chung-Hoon;Kang, Byung-Moon;Kim, Moon-Kyoo
    • Clinical and Experimental Reproductive Medicine
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    • v.30 no.4
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    • pp.309-316
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    • 2003
  • 연구목적: 스테로이드 계통의 에스트로겐 호르몬은 막 수용체와 결합하고 DNA에 부착되어, 자궁조직에서 발현되는 많은 유전자들의 발현 양상을 조절하는 것으로 알려져 있다. 본 연구에서는 난소를 제거한 생쥐 모델을 이용하여 에스트로겐에 의해 조절되는 전사 관련 유전자(transcription factor)들을 동정하고, early up-regulation gene으로 확인된 Fos related antigen (Fra1과 Fra2) 유전자의 발현 양상을 RT-PCR과 면역염색방법으로 살펴보았다. 연구재료 및 방법: 난소 절제술을 시행한 생쥐에 에스트로겐을 피하주사하고 2, 4, 6, 12시간 간격으로 자궁조직을 적출하였다. 대조군으로는 sesame oil만을 주사한 후 2시간째에 수획한 자궁조직을 사용하였으며, 시간대별로 채취한 자궁조직(n=4)에서 RT-PCR을 수행하였다. RT-PCR을 통해 early response gene으로 확인된 Fra1과 Fra2에 대한 에스트로겐의 영향을 살펴보기 위해 estrogen receptor antagonist인 ICI 182, 780을 주사하여 유전자 발현 양상의 변화를 살펴보았다. 또한, 자궁조직내에서의 단백질 발현 부위를 관찰하기 위해 면역조직화학염색을 실시하였다. 결 과: 생쥐 자궁조직에서 에스트로겐에 의해 발현 양상의 변화가 확인된 유전자는 early up-regulation genes (CREB2, Fra-1, 2, GATA5), late up-regulation gene (E2F1), no response genes (CREB1, ATF1, GLI3, E2F3), down-regulation genes (GLI2, E2F5, GATA-2, 3, 6) 등으로 구분할 수 있었다. 그 중 early up-regulation genes에 해당하는 Fra1과 Fra2 유전자는 ICI 182, 780에 의해 그 발현이 유의하게 감소되는 것을 확인하였다(p < 0.01). 이들 단백질은 생쥐 자궁조직의 상피세포층, 기질층, 근육층에서 고루 발현되었으며, 특히 근육층에서 강한 염색정도를 관찰할 수 있었다. 결 론: 이상의 결과를 통해 Fra1과 Fra2 유전자의 발현은 에스트로겐에 의해 조절됨을 알 수 있었으며, 이들의 강한 발현이 자궁조직의 근육층에서 관찰되어 이들의 기능에 대한 연구가 필요할 것으로 생각된다.

TM-25659-Induced Activation of FGF21 Level Decreases Insulin Resistance and Inflammation in Skeletal Muscle via GCN2 Pathways

  • Jung, Jong Gab;Yi, Sang-A;Choi, Sung-E;Kang, Yup;Kim, Tae Ho;Jeon, Ja Young;Bae, Myung Ae;Ahn, Jin Hee;Jeong, Hana;Hwang, Eun Sook;Lee, Kwan-Woo
    • 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.

Mapping of Human Cytomegalovirus IE1 Responsive Elements in the c-jun Promoter (사람세포거대바이러스 (Human Cytomegalovirus)의 극초기항원-1 (Immediate Early-1, IE-1)에 반응하는 c-jun Promoter의 유전자 지도 분석)

  • Park, Chung-Gyu;Han, Tae-Hee;Kim, Dae-Joong;Kim, Jin-Hee;Hwang, Eung-Soo;Choi, Sung-Bae;Cha, Chang-Yong
    • The Journal of Korean Society of Virology
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    • v.28 no.3
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    • pp.267-274
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    • 1998
  • Human cytomegalovirus (HCMV) has the ability to activate the expression of many viral and cellular genes. Among various viral proteins, the immediate early proteins (IE1-72kDa, IE2-86kDa) have been known to be potent transactivators. The product of c-jun proto-oncogene is important in cell activation and differentiation. Here, we tried to find out if the IE could activate the c-jun promoter and also tried to identify the responsible sequence elements in the c-jun activation by IE1-72kDa. We found HCMV IE expression transactivated the c-jun promoter in human embryonal lung fibroblasts (HEL). The activation fold by IE1-72kDa, IE2-86kDa and IE2-55kDa was 23, 35, and 5, respectively. When the expression of each IE was combined, it showed synergism. Expression of (IE1-72kDa + IE2-86kDa) and (IE1-72kDa + IE2-86kDa + IE2-55kDa) resulted in 131 and 162 fold increase, respectively. The c-jun promoter region between -117 and -59 contains binding sites for the transcription factors Spl, CAAT, AP-l like (ATF/CREB), and MEF2. Transient expression assays were performed using various reporter plasmids containing the c-jun promoter-regulatory region linked to the luciferase gene and a plasmid expressing HCMV IE1 gene. Deletional and point mutational analysis showed that the sequence between -225 to -160 and the CTF binding site were involved in the up-regulation of c-jun promoter.

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GENE EXPRESSION PATTERNS INDUCED BY $TAXOL^{(R)}$ AND CYCLOSPORIN A IN ORAL SQUAMOUS CELL CARCINOMA CELL LINE USING CDNA MICROARRAY (cDNA Microarray를 이용한 구강편평세포암종 세포주에서 $Taxol^{(R)}$과 Cyclosporin A로 유도된 유전자 발현양상)

  • Kim, Yong-Kwan;Lee, Jae-Hoon;Kim, Chul-Hwan
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.28 no.3
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    • pp.202-212
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    • 2006
  • It is well-known that paclitaxel($Taxol^{(R)}$), which is extracted from the pacific and English yew, has been used as a chemotherapeutic agent for ovarian carcinoma and advanced breast carcinoma and Cyclosporin A, which is highly lipophilic cyclic peptide and isolated from a fungus, has been also used as an useful immunosuppressive drug after transplantation and is associated with cellular apoptosis. Since 1953, in which James Watson, Rosalind Franklin and Francis Crick discovered the double helical structure of DNA, a few kinds of techniques for identifying gene expression have been developed. In postgenomic period, many of researchers have used the DNA microarray which is high throughput screening technique to screen large numbers of gene expression simultaneously. In this study, we searched and screened the gene expression in the oral squamous cell carcinoma cell lines treated with $Taxol^{(R)}$, cyclosporin or cyclosporin combined with $Taxol^{(R)}$ using cDNA microarray. The results were as following; 1. It was useful that the appropriate concentration of Cyclosporin A and $Taxol^{(R)}$ used in oral squamous cell carcinoma cell line was under 1${\mu}g/ml$ and 3${\mu}g/ml$. 2. In the experimental group in which $Taxol^{(R)}$ and $Taxol^{(R)}$ + Cyclosporin A were used, the cell growth was extremely decreased. 3. In the group in which Cyclosporin A was used, the MTT assay was rarely decreased which means the activity of succinyl dehydrogenase is remained in mitochondria but in the group in which the mixture of Cyclosporin A and $Taxol^{(R)}$ were used, the MTT assay was extremely decreased. 4. In the each group in which Cyclosporin A(3 ${\mu}g/ml$) and $Taxol^{(R)}$(1 ${\mu}g/ml$) were used, the cell arrest was appeared in $G_2/M$ phase and in the group in which $Taxol^{(R)}$(3 ${\mu}g/ml$) was used, the cell arrest was appeared in both S phase and $G_2/M$ phase. 5. In the oral squamous cell carcinoma cell line treated with $Taxol^{(R)}$, several genes including ANGPTL4, RALBP1 and TXNRD1, associated with apoptosis, SUI1, MAC30, RRAGA and CTGF, related with cell growth, HUS1 and DUSP5, related with cell cycle and proliferation, ATF4 and CEBPG, associated with transcription factor, BTG1 and VEGF, associated with angiogenesis, FDPS, FCER1G, GPA33 and EPHA4 associated with signal transduction and receptor activity and AKR1C2 and UGTA10 related with carcinogenesis were detected in increased levels. The genes that showed increaced expression in the oral squamous cell carcinoma cell line treated with Cyclosporin A were CYR61, SERPINB2, SSR3 and UPA3A which are known as genes associated with cell growth, carcinogenesis, receptor activity and transcription factor. The genes expressed in the HN22 cell line treated with cyclosporin combined with $taxol^{(R)}$ were ALCAM and GTSE1 associated with cancer invasiveness and cell cycle regulation.