• Proceedings of the Korean Vacuum Society Conference
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• 2016.02a
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• pp.263-263
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• 2016

최근 반도체 시장에서는 저비용으로 고성능 박막 트랜지스터(TFT)를 제작하기 위한 다양한 기술들이 연구되고 있다. 먼저, 재료적인 측면에서는 비정질 상태에서도 높은 이동도와 가시광선 영역에서 투명한 특성을 가지는 산화물 반도체가 기존의 비정질 실리콘이나 저온 폴리실리콘을 대체하여 차세대 디스플레이의 구동소자용 재료로 많은 주목받고 있다. 또한, 공정적인 측면에서는 기존의 진공장비를 이용하는 PVD나 CVD가 아닌 대기압 상태에서 이루어지는 용액 공정이 저비용 및 대면적화에 유리하고 프리커서의 제조와 박막의 증착이 간단하다는 장점을 가지기 때문에 활발한 연구가 이루어지고 있다. 특히 산화물 반도체 중에서도 indium-gallium-zinc oxide (IGZO)는 비교적 뛰어난 이동도와 안정성을 나타내기 때문에 많은 연구가 진행되고 있지만, 산화물 반도체 기반의 박막 트랜지스터가 가지는 문제점 중의 하나인 문턱전압의 불안정성으로 인하여 상용화에 어려움을 겪고 있다. 따라서, 본 연구에서는 기존의 산화물 반도체의 불안정한 문턱전압의 문제점을 해결하기 위해 마이크로웨이브 열처리를 적용하였다. 또한, 기존의 IGZO에서 suppressor 역할을 하는 값비싼 갈륨(Ga) 대신, 저렴한 지르코늄(Zr)과 하프늄(Hf)을 각각 적용시켜 용액 공정 기반의 Zr-In-Zn-O (ZIZO) 및 Hf-In-Zn-O (HIZO) TFT를 제작하여 시간에 따른 문턱 전압의 변화를 비교 및 분석하였다. TFT 소자는 p-Si 위에 습식산화를 통하여 100 nm 두께의 $SiO_2$가 열적으로 성장된 기판 위에 제작되었다. 표준 RCA 세정을 진행하여 표면의 오염 및 자연 산화막을 제거한 후, Ga, Zr, Hf 각각 suppressor로 사용한 IGZO, ZIZO, HIZO 프리커서를 이용하여 박막을 형성시켰다. 그 후 소스/드레인 전극 형성을 위해 e-beam evaporator를 이용하여 Ti/Al을 5/120 nm의 두께로 증착하였다. 마지막으로, 후속 열처리로써 마이크로웨이브와 퍼니스 열처리를 진행하였다. 그 결과, 기존의 퍼니스 열처리와 비교하여 마이크로웨이브 열처리된 IGZO, ZIZO 및 HIZO 박막 트랜지스터는 모두 뛰어난 안정성을 나타냄을 확인하였다. 결론적으로, 본 연구에서 제안된 마이크로웨이브 열처리된 용액공정 기반의 ZIZO와 HIZO 박막 트랜지스터는 추후 디스플레이 산업에서 IGZO 박막 트랜지스터를 대체할 수 있는 저비용 고성능 트랜지스터로 적용될 것으로 기대된다.

• Molecules and Cells
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• v.38 no.6
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• pp.548-561
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• 2015

By combining conventional single cell analysis with flow cytometry and public database searches with bioinformatics tools, we extended the expression profiling of thymic stromal cotransporter (TSCOT), Slc46A2/Ly110, that was shown to be expressed in bipotent precursor and cortical thymic epithelial cells. Genome scale analysis verified TSCOT expression in thymic tissue- and cell type- specific fashion and is also expressed in some other epithelial tissues including skin and lung. Coexpression profiling with genes, Foxn1 and Hoxa3, revealed the role of TSCOT during the organogenesis. TSCOT expression was detected in all thymic epithelial cells (TECs), but not in the $CD31^+$endothelial cell lineage in fetal thymus. In addition, ABC transporter-dependent side population and Sca-$1^+$ fetal TEC populations both contain TSCOT-expressing cells, indicating TEC stem cells express TSCOT. TSCOT expression was identified as early as in differentiating embryonic stem cells. TSCOT expression is not under the control of Foxn1 since TSCOT is present in the thymic rudiment of nude mice. By searching variations in the expression levels, TSCOT is positively associated with Grhl3 and Irf6. Cytokines such as IL1b, IL22 and IL24 are the potential regulators of the TSCOT expression. Surprisingly, we found TSCOT expression in the lung is diminished in lung cancers, suggesting TSCOT may be involved in the suppression of lung tumor development. Based on these results, a model for TEC differentiation from the stem cells was proposed in context of multiple epithelial organ formation.

• BMB Reports
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• v.43 no.2
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• pp.97-102
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• 2010

Clenbuterol, a $\beta_2$-adrenoceptor agonist, has been proven to be a powerful repartition agent that can decrease fat deposition. Based on results from our previous cDNA microarray experiment of pig clenbuterol administration, a novel up-regulated EST was full-length cloned (4859 bp encoding 1041 amino acids) and found to be the pig homolog of large tumor suppressor 2 (Lats2). We mapped pig Lats2 to chromosome 11p13-14 by using FISH, and western blotting demonstrated that pig Lats2 protein was most abundant in adipose. In Drosophila, Lats2 ortholog was reported as a key component of the Hippo pathway which regulates cell differentiation and growth. Here, we show that pig Lats2 exhibit inverted expression to YAP1, another member of the Hippo pathway which positively regulates cell growth and proliferation, during the differentiation of 3T3-L1 preadipocytes. Our results suggested that Lats2 may involve in Hippo pathway regulating the fat reduction by inhibiting adipocyte differentiation and growth.

• The Plant Pathology Journal
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• v.27 no.4
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• pp.315-323
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• 2011

Soybean plants infected with Bean pod mottle virus (BPMV) develop acute symptoms that usually decrease in severity over time. In other plant-virus interactions, this type of symptom recovery has been associated with degradation of viral RNAs by RNA silencing, which is accompanied by the accumulation of virus-derived small interfering RNAs (siRNAs). In this study, changes in the accumulation of BPMV siRNAs were investigated in soybean plants infected with BPMV alone, or infected with both BPMV and Soybean mosaic virus (SMV) and in transgenic soybean plants expressing SMV helper component-protease (HC-Pro). In many potyviruses, HC-Pro is a potent suppressor of RNA silencing. In plants infected with BPMV alone, accumulation of siRNAs was positively correlated with symptom severity and accumulation of BPMV genomic RNAs. Plants infected with both BPMV and SMV and BPMV-infected transgenic soybean plants expressing SMV HC-Pro exhibited severe symptoms characteristic of BPMVSMV synergism, and showed enhanced accumulation of BPMV RNAs and siRNAs compared to plants infected with BPMV alone and nontransgenic plants. Likewise, SMV HC-Pro enhanced the accumulation of siRNAs produced from a silenced green fluorescent protein gene in transient expression assays, while the P19 silencing suppressor of Tomato bushy stunt virus did not. Consistent with the modes of action of HC-Pro in other systems, which have shown that HC-Pro suppresses RNA silencing by preventing the unwinding of duplex siRNAs and inhibiting siRNA methylation, these studies showed that SMV HC-Pro interfered with the activities of RNA-induced silencing complexes, but not the activities of Dicer-like enzymes in antiviral defenses.

• Journal of Oriental Neuropsychiatry
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• v.18 no.1
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• pp.95-110
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• 2007

Objective : The purpose of this study was to investigate molecular basis of neuroprotective effect in total ginsenosides. After H202 induced neurotoxicity, gene expression profiling of SH-SY5Y neuroblastoma cells treated by total ginsenosides is analyzed. Method : After SH-SY5Y cells were cultured, they were damaged by H202 induced oxidative stress. After twenty four hours, experimental group is treated by total ginsenosides and control group is treated by 0.9% saline. A high density cDNA microarray chip is used to analyze the gene expression profiling of SH-SY5Y cells. The Significance Analysis of Microarray method is used for identifying genes on a microarray. Results : 1. According to the results of microarray experiment, 17 genes were up-regulated, 38 genes were down-regulated. 2. Expression of OPHNl, KTANl, ATM, PRKCE, MAPKs genes associated with cell proliferation, neural growth, and the prevention of apoptosis were increased. 3. Change of EPX gene was the greatest among all genes. EPX gene associated with oxidative stress, and tumor suppressor gene ADAM11 were decreased. Conclusion : According to this study, molecular basis of neuroprotective effect of total ginsenosides is as followings: the increase of gene expression associated with cell proliferation, neuron growth, the prevention of apoptotsis and decrease of gene expression associated with oxidative stress and tumor suppressor.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.178-178
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• 1994

Hepatitis B Virus (HBV) is a DNA virus with a 3.2kb partially double-stranded genome. The life cycle of the virus involves a reverse transcription of the greater than genome length 3.5kb mRNA. This pegenomic RNA contains all the genetic information encoded by the virus and functions as an intermediate in viral replication. Tumor suppressor p53 has previously been shown to interact with the X-gene product of the HBV, which led us to hypothesize that p53 may act as a negative regulator of HBV replication and the role of the X-gene product is to overcome the p53-mediated restriction. As a first step to prove the above hypothesis, we tested whether p53 represses the propagation of HBV in in vitro replication system. By transient cotransfection of the plasmid containing a complete copy of the HBV genome and/or the plasmid encoding p53, we found that the replication of HBV is specifically blocked by wild-type p53. The levels of HBV DNA, HBs Ag and HBc/e Ag secreted in cell culture media were dramatically reduced upon coexpresion of wild-type p53 but not by the coexpression of the mutants of p53 (G154V and R273L). Furthermore, levels of RNAs originated from HBV genome were repressed more than 10 fold by the cotransfection of the p53 encoding plasmid. These results clearly states that p53 is a nesative regulator of the HBV replication. Next, to addresss the mechanism by which p53 represses the HBV replication, we performed the transient transfection experiments employing the pregenomic/core promoter-CAT(Chloramphenicol Acetyl Transferase) construct as a reporter. Cotransfection of wild-type p53 but not the mutant p53 expression plasmids repressed the CAT activity more than 8 fold. Integrating the above results, we propose that p53 represses the replication of HBV specifically by the down-regulation of the pregenomic/core promoter, which results in the reduced DNA synthesis of HBV. Currently, the mechanism by which HBV overcomes the observed p53-mediated restriction of replication is tinder investigation.

• The Journal of the Korean bone and joint tumor society
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• v.9 no.1
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• pp.77-83
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• 2003

Aggressive fibromatosis is a rare soft tissue tumor with locally invasive and infiltrative characteristics. The mechanism of this invasive nature was not reported until now. Mutations or reduction of PTEN, tumor suppressor gene, in cancer tissues, have been found to be associated with invasiveness and metastatic properties of cancer cells. To know the pattern of expression of PTEN in aggressive fibromatosis, we analysed the expression of PTEN with immunohistochemical stain and immunoblotting. PTEN was homogeneously expressed in the normal musculoaponeurotic tissues, but absent or very faint in tissues of patients with aggressive fibromatosis as evidenced by western blot analysis and immunohistochemical examinations. Although the meaning of decreased PTEN expression in aggressive fibromatosis is not certain, it might be involved in the growth of the aggressive fibromatosis, and associated with phenotype of aggressive fibromatosis.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.3
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• pp.297-304
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• 2016

Klotho functions as a tumor suppressor predominantly expressed in renal tubular cells, the origin of clear cell renal cell carcinoma (ccRCC). Altered expression and/or activity of growth factor receptor have been implicated in ccRCC development. Although Klotho suppresses a tumor progression through growth factor receptor signaling including insulin-like growth factor-1 receptor (IGF-1R), the role of Klotho acting on IGF-1R in ccRCC and its clinical relevance remains obscure. Here, we show that Klotho is favorable prognostic factor for ccRCC and exerts tumor suppressive role for ccRCC through inhibiting IGF-1R signaling. Our data shows the following key findings. First, in tumor tissues, the level of Klotho and IGF-1R expression are low or high, respectively, compared to that of adjacent non-neoplastic parenchyma. Second, the Klotho expression is clearly low in higher grade of ccRCC and is closely associated with clinical outcomes in tumor progression. Third, Klotho suppresses IGF-1-stimulated cell proliferation and migration by inhibiting PI3K/Akt pathway. These results provide compelling evidence supporting that Klotho acting on IGF-1R signaling functions as tumor suppressor in ccRCC and suggest that Klotho is a potential carcinostatis substance for ccRCC.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.16
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• pp.6581-6586
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• 2014

Background: The istone deacetylase (HDAC) inhibitor trichostatin A (TSA) is known to mediate the regulation of gene expression and antiproliferation activity in cancer cells. Kr$\ddot{u}$ppel-like factor 4 (klf4) is a zinc finger-containing transcription factor of the SP/KLF family, that is expressed in a variety of tissues and regulates cell proliferation, differentiation, tumorigenesis, and apoptosis. It may either either function as a tumor suppressor or an oncogene depending on genetic context of tumors. Aims: In this study, we tested the possibility that TSA may increase klf4 expression and cancer cell growth inhibition and apoptosis in SKOV-3 and A549 cells. Materials and Methods: The cytotoxicity of TSA was determined using the MTT assay test, while klf4 gene expression was assessed by real time PCR andto ability of TSA to induce apoptosis using a Vybrant Apoptosis Assay kit. Results: Our results showed that TSA exerted dose and time dependent cytotoxicity effect on SKOV-3 and A549 cells. Moreover TSA up-regulated klf4 expression. Flow cytometric analysis demonstrated that apoptosis was increased after TSA treatment. Conclusions: Taken together, this study showed that TSA increased klf4 expression in SKOV3 and A549 cell lines, consequently, klf4 may played a tumor-suppressor role by increasing both cell growth inhibition and apoptosis. This study sheds light on the details of molecular mechanisms of HDACI-induced cell cycle arrest and apoptosis.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7583-7586
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• 2013

Background: Suppressor of cytokine signaling (SOCS)-1 acts as a key regulator of many cytokine signaling pathways and its abnormal expression has been identified in several human malignancies, suggesting potential roles in carcinogenesis. The aim of this study was to investigate any association between the functional SOCS-1 -1478CA>del polymorphism and colorectal cancer (CC) as well as age at onset in a Turkish clinical sample. Materials and Methods: A total of 122 subjects were enrolled in this case-control study (70 CC cases and 52 controls). The SOCS-1 -1478CA>del polymorphism was genotyped using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results: The odds ratio of the del allele for CC relative to the CA allele was not significantly different between the groups (OR=0.71, 95% CI=0.41-1.22, p=0.27). This result did not change after adjustment for age and sex on multivariable regression analysis (OR=0.84, 95% CI=0.59-1.34, p=0.53). When the SOCS-1 -1478CA>del polymorphism was analyzed among CC patients in relation to the age at disease onset, we found no significant differences between subjects with the del/del, CA/del, and CA/CA genotypes. Conclusions: The results of our study did not point towards a major role of the SOCS-1 -1478CA>del polymorphism in the pathogenesis of CC in Turkish subjects.