• Journal of Life Science
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• v.32 no.11
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• pp.833-840
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• 2022

Chronic inflammation has been shown to be closely associated with tumor development and progression. Nuclear factor kappa B (NF-κB) is composed of a family of five transcription factors. NF-κB signaling plays a crucial role in the inflammatory response and is often found to be dysregulated in various types of cancer, making it an attractive target in cancer therapeutics. In this study, CDC-like kinase 3 (CLK3) was identified as a novel kinase that regulates the NF-κB signaling pathway. Our data demonstrate that CLK3 inhibits the canonical and non-canonical NF-κB pathways. Luciferase assays following the transient or stable expression of CLK3 indicated that this kinase inhibited NF-κB activation mediated by Tumor necrosis factor-alpha (TNFα) and Phorbol 12-myristate 13-acetate (PMA), which are known to activate NF-κB signaling via the canonical pathway. Consistent with data on the ectopic expression of CLK3, CLK3 knockdown using shRNA constructs increased NF-κB activity 1.5-fold upon stimulation with TNFα in HEK293 cells compared with the control cells. Additionally, overexpression of CLK3 suppressed the activation of this signaling pathway induced by NF-κB-inducing kinase (NIK) or CD40, which are well-established activators of the non-canonical pathway. To further examine the negative impact of CLK3 on NF-κB signaling, we performed Western blotting following the TNFα treatment to directly identify the molecular components of the NF-κB pathway that are affected by this kinase. Our results revealed that CLK3 mitigated the phosphorylation/activation of transforming growth factor-α-activated kinase 1 (TAK1), inhibitor of NF-κB kinase alpha/beta (IKKα/α), NF-κB p65 (RelA), NF-κB inhibitor alpha (IκBα), and Extracellular signal-regulated kinase 1/2-Mitogen-activated protein kinase (ERK1/2-MAPK), suggesting that CLK3 inhibits both the NF-κB and MAPK signaling activated by TNFα exposure. Further studies are required to elucidate the mechanism by which CLK3 inhibits the canonical and non-canonical NF-κB pathways. Collectively, these findings reveal CLK3 as a novel negative regulator of NF-κB signaling.

• Applied Chemistry for Engineering
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• v.26 no.2
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• pp.154-158
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• 2015

In this study, the catalytic activity of ${\gamma}-Al_2O_3$ was investigated for the decomposition of $NF_3$. Reactions for $NF_3$ decomposition were carried out in the range of reaction temperature of $330{\sim}730^{\circ}C$ and GHSV of $3,000{\sim}15,000mL/g-cat{\cdot}h$ in a fixed-bed catalytic reactor system. Thermal decomposition of $NF_3$ was also performed in order to compare with the catalytic decomposition of $NF_3$. The conversion of $NF_3$ by the catalytic decomposition at $400^{\circ}C$ was four times higher than that of the thermal decomposition. It was confirmed that the reaction behavior of $NF_3$ over ${\gamma}-Al_2O_3$ exhibited two reaction pathways in the presence of steam. Fluorine in $NF_3$ over ${\gamma}-Al_2O_3$ was chemically absorbed to $AlF_3$ by the gas-solid reaction in the absence of steam. The catalytic decomposition of $NF_3$ occurred by hydrolysis with steam. It was also confirmed by FT-IR analysis that $NF_3$ was completely decomposed to NOx and HF above $500^{\circ}C$.

• Journal of Acupuncture Research
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• v.27 no.3
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• pp.1-13
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• 2010

목적 : 이 연구는 봉약침의 봉독과 그 주요성분인 멜리틴이 NF-${\kappa}B$의 활성억제와 세포자멸사 관련 단백질의 발현 조절을 통하여 세포자멸사를 유도함으로써 전립선 암세포주인 PC-3 세포의 성장을 억제하는지를 확인하고 해당 기전을 살펴보고자 하였다. 방법 : 봉독이나 멜리틴을 처리한 후 PC-3의 성장억제를 관찰하기 위해 WST-1 assay, CCK-8 assay를 시행하였고, 세포자멸사 조절단백질의 변동 관찰에는 western blot analysis를 시행하였고, 세포자멸사와 연관된 NF-${\kappa}B$의 활성 변화를 관찰하기 위해 EMSA를 시행하였으며, PC-3에서 봉독이나 멜리틴과 NF-${\kappa}B$의 상호작용을 관찰하기 위해 transient transfection assay를 시행하여 세포생존율과 NF-${\kappa}B$의 활성 변동을 측정하였다. 결과 : PC-3 세포에 봉독이나 멜리틴을 처리한 후, 전립선암세포의 성장, 세포자멸사의 유발, 세포자멸사 관련 단백질의 발현, NF-${\kappa}B$의 활성, NF-${\kappa}B$의 p50, $IKK{\alpha}$, $IKK{\beta}$ 치환 후 NF-${\kappa}B$의 활성과 PC-3 세포 증식에 미치는 영향을 관찰하여 다음과 같은 결과를 얻었다. 1. PC-3 세포에서 봉독이나 멜리틴을 처리한 후 세포자멸사가 유도되어 세포성장이 억제되었고, 세포자멸사 관련 단백질 중 분리된 PARP, caspase-3, -9는 유의한 증가를, Bcl-2, XIAP, cXIAP2는 유의한 감소를 나타내었다. 2. PC-3 세포에서 봉독이나 멜리틴을 처리한 후 NF-${\kappa}B$의 활성은 유의한 감소를 나타내었다. 3. PC-3 세포에서 NF-${\kappa}B$의 p50, $IKK{\alpha}$, $IKK{\beta}$를 치환하여 작용기를 없애고 봉독이나 멜리틴을 처리하였을 경우에도 NF-${\kappa}B$의 활성이 유의한 감소를 나타내었다. 결론 : 이상의 결과는 봉독이나 멜리틴이 NF-${\kappa}B$의 활성 억제를 통하여 인간 전립선암세포주인 PC-3의 세포자멸사를 유발함으로써 증식억제 효과가 있음을 입증한 것으로, 전립선암의 예방과 치료에 대한 효과적인 치료제 개발에 도움이 될 것으로 기대된다.

• Parasites, Hosts and Diseases
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• v.30 no.1
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• pp.33-42
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• 1992

Naegleria fowleri, a free-living amoeba commonly found in moist soil and fresh water, enters the body via the nasal mucosa and migrates along the olfactory nerve to t he brain, where it causes acute amoebic meningoencephalitis. In the present study 7 clones secreting monoclonal antibodies (McAbs) against N. fowleri were produced and the effector function of them was investigated. Their isotopes were IgGl (Nf 1, Nf 154), 19G3 (Nf 137) and 19A (Nf 1, Nf 2, Nf 256, Nf 279). Five McAbs (McAb Nf 2, Nf 279, Nf 27, Nf 154, Nf 137) were specific for N. fowleri by ELISA and recognized the antigenic determinants located on the trophoBoite surface by IFAT and immunoperoxidase stain. These aye McAbs had capacity to agglutinate N. fowleri trophozoites and inhibited the growth of the amoeba in culture medium. McAb Nf 2 inhibited proliferation of trophozoites in vitro significantly. Also the cytotoxicity of JV. fowleri against CHO cell was reduced in the presence of McAb Nf 2 and McAb Nf 154. From these results McAb Nf 2 was confirmed to weaken the virulence of the amoeba among 7 screened McAbs.

• Journal of the Korean earth science society
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• v.39 no.6
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• pp.519-532
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• 2018

We investigated the effect of galactic plane toward molecular motion and kinematics in the northern filament (NF) of Orion Molecular Clouds Complex (OMC) using $^{12}CO$ (J=1-0) line. Observed data were from three areas including NF1, NF2, and NF3 in far-out order from galactic plane, for a total 270 hours by Seoul National University Radio Astronomy Observatory (SRAO) 6m telescope, with 2arcmin spatial resolution. galactic plane and OMC NF were connected to each other along the magnetic field at a density of 3% for $^{12}CO$ (J=2-1) and 9% for the case of dust. $^{12}CO$ (J=1-0), $^{12}CO$ (J=2-1), and interstellar dusts were distributed uniformly in NF3, but only in certain regions with relatively high density in NF1 and NF2. NF showed a single structure, partial shrinking motion in NF1, and rotational motion at the bottom of NF2, and spiral rotation associated with magnetic field only in NF3. The position-velocity analysis showed that the materials including $^{12}CO$ (J=1-0) could flow toward galactic plane along NF2 and NF3. However, there was no clear cause for the material to flow toward galactic plane in this result. Further detailed observation for rotational motion at the top of NF1 and NF2 might help to confirm it.

• Molecules and Cells
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• v.20 no.2
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• pp.241-246
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• 2005

PDK-1 activates PI3-kinase/Akt signaling and regulates fundamental cellular functions, such as growth and survival. NF-${\kappa}B$ is involved in the induction of a variety of cellular genes affecting immunity, inflammation and the resistance to apoptosis induced by some anti-cancer drugs. Even though the crucial involvement of the PI3-kinase/Akt pathway in the anti-apoptotic activation of NF-${\kappa}B$ is well known, the exact role of PDK-1 as well as PI3-kinase/Akt in NF-vactivation is not understood. Here we demonstrate that PDK-1 plays a pivotal role in transcriptional activation of NF-${\kappa}B$ by dissociating the transcriptional co-repressor HDAC1 from the p65 subunit of NF-${\kappa}B$. The association of CBP with p65 was not directly modulated by PDK-1 or by PI3-kinase. Etoposide activated NF-${\kappa}B$ through PI3-kinase/Akt, and the transcription activation domain (TAD) of p65 was further activated by wild-type PDK-1. Overexpression of a dominant negative PDK-1 mutant decreased etoposide-induced NF-${\kappa}B$ transcription and further down-regulated the ectopic HDAC1-mediated decrease in NF-${\kappa}B$ transcriptional activity. Thus activation of PDK-1 relieves the HDAC1-mediated repression of NF-${\kappa}B$ that may be related to basal as well as activated transcription by NF-${\kappa}B$. This effect may also explain the role of the PI3-kinase/PDK-1 pathway in the anti-apoptotic function of NF-${\kappa}B$ associated with the chemoresistance of cancer cells.

• Journal of the Semiconductor & Display Technology
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• v.17 no.4
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• pp.97-100
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• 2018

$NF_3$ Plasma etching of silicon was conducted by injecting only $NF_3$ gas into reactive ion etching. $NF_3$ Plasma etching was done in intermediate pressure. Silicon etching by $NF_3$ plasma in reactive ion etching was diagnosed through residual gas analyzer and optical emission spectroscopy. In plasma etching, optical emission spectroscopy is generally used to know what kinds of species in plasma. Also, residual gas analyzer is mainly to know the byproducts of etching process. Through experiments, the results of optical emission spectroscopy during silicon etching by $NF_3$ plasma was analyzed with connecting the results of etch rate of silicon and residual gas analyzer. It was confirmed that $NF_3$ plasma etching of silicon in reactive ion etching accords with the characteristic of reactive ion etching.

• BMB Reports
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• v.43 no.12
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• pp.807-812
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• 2010

$NF{\kappa}B$ and ZAS3 are transcription factors that control important cellular processes including immunity, cell survival and apoptosis. Although both proteins bind the ${\kappa}B$-motif, they produce opposite physiological consequences; $NF{\kappa}B$ activates transcription, promotes cell growth and is often found to be constitutively expressed in cancer cells, while ZAS3 generally represses transcription, inhibits cell proliferation and is downregulated in some cancers. Here, we show that ZAS3 inhibits $NF{\kappa}B$-dependent transcription by competing with $NF{\kappa}B$ for the ${\kappa}B$-motif. Transient transfection studies show that N-terminal 645 amino acids is sufficient to repress transcription activated by $NF{\kappa}B$, and that the identical region also possesses intrinsic repression activity to inhibit basal transcription from a promoter. Finally, in vitro DNA-protein interaction analysis shows that ZAS3 is able to displace $NF{\kappa}B$ by competing with $NF{\kappa}B$ for the ${\kappa}B$-motif. It is conceivable that ZAS3 has therapeutic potential for controlling aberrant activation of $NF{\kappa}B$ in various diseases.

• The Bulletin of The Korean Astronomical Society
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• v.43 no.2
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• pp.52.1-52.1
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• 2018

Orion Molecular Clouds Complex(OMC) 분자운에는 별 생성은 없으면서 은하면 방향으로 누워있는 큰 규모($10^{\circ}{\times}0.5^{\circ}$)의 필라멘트 구조가 있다. 본 연구는 북쪽 필라멘트(이하 NF)를 대상으로 12CO (J = 1-0) 선 관측 데이터를 이용하여 필라멘트의 운동학적 연구를 수행함으로서 은하면과의 상관관계를 알아보고자 하였다. 관측은 공간분해능은 2 arcmin인 SRAO(Seoul Radio Astronomy Observatory)의 6m 밀리미터 망원경이 사용되었고 큰 규모로 인해 은하면으로부터 먼 순서로 NF1, NF2, NF3 세 곳으로 관측 지역이 정해졌다. 연구결과 필라멘트는 매우 낮은 수준의 12CO (J = 2-1)과 티끌 분포에서 자기장을 따라 은하면 방향으로 연계되어 보였다. 밀도 분포에서는 SRAO 12CO (J = 1-0) 적분강도와 Planck 위성의 12CO (J = 2-1)과 티끌 자료를 이용했을 때, 12CO와 성간 티끌은 주로 은하면에 수직인 방향에서 밀도가 높았다. 속도 분포와 위치 속도 분석을 통해 NF는 단일 구조의 분자운 형태이고 NF2 하단에서는 회전 운동의 가능성이 확인되었다. NF3는 자기장에 의해 생성된 나선형 회전을 하고 있으며, NF2와 NF3를 따라 은하면을 향하여 12CO (J = 1-0)를 비롯한 물질이 흐르고 있음도 확인되었다. 하지만 은하면을 향하여 물질이 흐르는 원인을 제공하는 천체가 무엇인지와 NF1과 NF2 상단의 회전 운동은 확인 할 수 없었으며 이들 지역에 대한 상세한 관측이 요구된다.

• Journal of Korean Society of Environmental Engineers
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• v.34 no.6
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• pp.391-396
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• 2012

The destruction study of $NF_3$ gas emitted from the semiconductor industry is performed with electron-beam technology. Absorbed dose (kGy) and current ranged from 0 (0) to 400 kGy (20 mA). The concentration of $NF_3$ gas ranged from 500 to 2,000 ppm. In order to assess the effect of a residence time on DRE (Destruction and Removal Efficiency, %), experiments also conducted at different irridiation times of 5 sec, 10 sec, 15 sec and 20 sec respectively. As absorbed dose and current increased, DRE of $NF_3$ was also increased. However, DRE (%) of $NF_3$ decreased with increasing the concentration of $NF_3$ gas. The DRE of $NF_3$ was about 90% at an absorbed dose of 400 kGy.