• Journal of Acupuncture Research
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• v.22 no.2
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• pp.133-139
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• 2005

Cobrotoxin, a venom of Vipera lebetina turanica, is a group of basic peptidescomposed of 233 amino acids with six disulfide bonds formed by twelve cysteins. NF-kB is activated by subsequent release of inhibitory IkB and translocation of p50. Since sulfhydryl group is present in kinase domain of p50 subunit of NF-kB, cobrotoxin could modify NF-kB activity by protein-protein interaction. We therefore examined effect of cobrotoxin on NF-kB activities in lipopolysaccharide (LPS) and sodium nitroprusside (SNP)-stimulated Raw 264.7 mouse macrophages. Cobrotoxin suppressed the LPS and SNP-induced release of IkB and p50 translocation resulted in inhibition of DNA binding activity of NF-kB. Inhibition of NF-kB resulted in reduction of the LPS and SNP-induced production of inflammatory mediators NO and PGE2 generation. The inhibitory effect of cobrotoxin on the NF-kB activity were blocked by addition of reducing agents dithiothreitol and glutathione. These results demonstrate that cobrotoxin inhibits activation of NF-kB, and suggest that pico to nanomolar range of cobrotoxin could inhibit the expression of genes in the NF-kB signal pathway.

• 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 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.

• Journal of Acupuncture Research
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• v.26 no.3
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• pp.39-48
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• 2009

목적 : 이 연구는 봉약침의 주요성분인 멜리틴이 NF-${\kappa}$B의 활성억제를 통하여 세포자멸사를 유도하고, 전립선 암세포주인 DU-145 세포의 성장을 억제하는지를 확인하고 멜리틴의 NF-${\kappa}$B 활성억제기전을 살펴보고자 하였다. 방법 : 멜리틴을 처리한 후 DU-145의 성장억제를 관찰하기 위해 WST-1 assay를 시행하였고, 세포자멸 사의 관찰에는 DAPI stairung assay를 통한 세포형태관찰을 시행하였으며, 염증관련유전자 발현 관찰에는 western blot analysis를 시행하였고, 세포자멸사와 연관된 NF-${\kappa}$B의 활성 변화를 관찰하기 위해 EMSA와 luciferase assay를 시행하였으며, DU-145에서 멜리틴과 NF-${\kappa}$B의 상호작용을 관찰하기 위해 transient transfection assay를 시행 시 세포생존율과 NF-${\kappa}$B의 활성 변동을 측정하였다. 결과 : DU-145 세포에 멜리틴을 처리한 후, 전립선암세포의 성장, 세포자멸사의 유발, 염중관련유전자 발현 및 NF-${\kappa}$B의 활성, NF-${\kappa}$B의 p50 치환 후 NF-${\kappa}$B의 활성과 DU-145 세포 증식에 미치는 영향을 관찰하여 다음과 같은 결과를 얻었다. 1. DU-145 세포에서 멜리틴을 처리한 후 세포자멸사가 유도되어 세포성장이 억제되었다. 2. DU-145 세포에서 멜리틴을 처리한 후 염증관련유전자 발현 및 NF-${\kappa}$B의 활성에 유의한 감소를 나타내었다. 3. DU-145 세포에서 NF-${\kappa}$B의 p50와 IKK들을 치환하여 작용기를 없애고 멜리틴을 처리하였을 경우에도 세포활성 및 NF-${\kappa}$B의 활성의 유의한 감소를 나타내었다.

• Journal of Genetic Medicine
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• v.21 no.1
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• pp.22-30
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• 2024

Purpose: Neurofibromatosis 1 (NF1) is one of the most common autosomal dominant diseases caused by heterozygous mutation in the NF1 gene. Mutation detection is complex owing to the large size of the NF1 gene, the presence of a high number of partial pseudogenes, and the great variety of mutations. We aimed to study the mutation spectrum of NF1 gene in Korean patients with NF1. Materials and Methods: We have analyzed total 69 unrelated patients who were clinically diagnosed with NF1. PCR and sequencing of the NF1 gene was performed in all unrelated index patients. Additionally, multiplex ligation-dependent probe amplification (MLPA) test of the NF1 and SPRED1 gene analysis (sequencing and MLPA test) were performed in patients with negative results from NF1 gene sequencing analysis. Results: Fifty-five different variants were identified in 60 individuals, including six novel variants. The mutations included 36 single base substitutions (15 missense and 21 nonsense), eight splicing mutations, 13 small insertion or deletions, and three gross deletions. Most pathogenic variants were unique. The mutations were evenly distributed across exon one through 58 of NF1, and no mutational hot spots were found. When fulfilling the National Institutes of Health criterion for the clinical diagnosis of NF1, the detection rate was 84.1%. Cafe-au-lait macules were observed in all patients with NF1 mutations. There is no clear relationship between specific mutations and clinical features. Conclusion: This study revealed a wide spectrum and genetic basis of patients with NF1 in Korea. Our results aim to contribute genetic management and counseling.

• 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 $500^{\circ}C$.

• Tuberculosis and Respiratory Diseases
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• v.46 no.2
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• pp.185-194
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• 1999

Background: NF-$\kappa$B is a characteristic transcriptional factor whose functional activity is determined by post-translational modification of protein and subsequent change of subcellular localization. The involvement of the NF-$\kappa$B family of the transcription factors in the control of such vital cellular functions as immune response, acute phase reaction, replication of certain viruses and development and differentiation of cells has been clearly documented in many previous studies. Several recent observations have suggested that the NF-$\kappa$B might also be involved in the carcinogenesis of some hematological and solid tumors. Investigating the possibility that members of the NF-$\kappa$B family participate in the molecular control of malignant cell transformation could provide invaluable information on both molecular pathogenesis and cancer-related gene therapy. Method: To determine the expression patterns and functional roles of NF-$\kappa$B family transcription factors in human lung cancer cell lines NCI-H792, NCI-H709, NCI-H226 and NCI-H157 were analysed by western blot, using their respective antibodies. The nuclear and the cytoplasmic fraction of protein extract of these cell lines were subsequently obtained and NF-$\kappa$B expression in each fraction was again determined by western blot analysis. The type of NF-$\kappa$B complex present in the cells was determined by immunoprecipitation. To detect the binding ability of cell-line nuclear extracts to the KB consensus oligonucleotide, electrophoretic mobility shift assay(EMSA) was performed. Results: In the cultured human lung cancer cell lines tested, transcription factors of the NF-$\kappa$B family, namely the p50 and p65 subunit were expressed and localized in the nuclear fraction of the cellular extract by western blot analysis and immunocytochemistry. Immunoprecipitation assay showed that in the cell, the p50 and p65 subunits made NF-$\kappa$B complex. Finally it was shown by Electrophoretic Mobility Shift Assay(EMSA) that nuclear extracts of lung cancer cell lines are able to bind to NF-$\kappa$B consensus DNA sequences. Conclusion: These data suggest that in human lung cancer cell lines the NF-$\kappa$B p50/p65 complex might be activated. and strengthen the hypothesis that NF-$\kappa$B family transcription factors might be involved in the carcinogenesis of human lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.55 no.5
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• pp.488-498
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• 2003

Background : Activation of the transcription factor NF-${\kappa}B$ has been shown to protect cells from tumor necrosis factor-alpha, chemotherapy, and radiation-induced apoptosis. NF-${\kappa}B$-dependent cIAP expression is a major antiapoptotic mechanism for that. NF-${\kappa}B$ activation and cIAP expression in A549 lung cancer cells which is relatively resistant to radiation-induced cell death were investigated for the mechanism of radioresistance. Materials and methods : We used A549 lung cancer cells and Clinac 1800C linear accelerator for radiation. Cell viability test was done by MTT assay. NF-${\kappa}B$ activation was tested by luciferase reporter gene assay, Western blot for $I{\kappa}B{\alpha}$ degradation, and electromobility shift assay. For blocking ${\kappa}B$, MG132 and transfection of $I{\kappa}B{\alpha}$-superrepressor plasmid construct were used. cIAP expression was analyzed by RT-PCR and cIAP2 promoter activity was performed using luciferase assay system. Results : MTT assay showed that cytotoxicity even 48 hr after radiation in A549 cells were less than 20%. Luciferas assay demonstrated weak NF-${\kappa}B$ activation of $1.6{\pm}0.2$ fold compared to PMA-induced $3.4{\pm}0.9$ fold. Radiation-induced $I{\kappa}B{\alpha}$ degradation was observed in Western blot and NF-${\kappa}B$ DNA binding was confirmed by EMSA. However, blocking NF-${\kappa}B$ using MG132 and $I{\kappa}B{\alpha}$-superrepressor transfection did not show any sensitizing effect for radiation-induced cell death. The result of RT-PCR for cIAP1 & 2 expression was negative induction while TNF-${\alpha}$ showed strong expression for cIAP1 & 2. The cIAP2 promoter activity also did not show any change compared to positive control with TNF-${\alpha}$. Conclusion : We conclude that activation of NF-${\kappa}B$ does not determine the intrinsic radiosensitivity of cancer cells, at least for the cell lines tested in this study.

• Proceedings of the Korean Radioactive Waste Society Conference
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• 2018.05a
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• pp.41-42
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• 2018

• Proceedings of the Korean Radioactive Waste Society Conference
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• 2018.05a
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• pp.62-63
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• 2018