• 한국동물학회:학술대회논문집
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• 한국동물학회 2003년도 한국생물과학협회 학술발표대회
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• pp.197.2-197
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• 2003

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• 한국진공학회:학술대회논문집
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• 한국진공학회 2012년도 제43회 하계 정기 학술대회 초록집
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• pp.407-407
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• 2012

화학기상증착법(CVD; Chemical Vapor deposition)으로 h-BN을 증착하여 성장 시간에 따른 표면의 특성 및 결정성을 연구하였다. 암모니아 보레인(BH3NH3)을 보론 나이트라이드(Boron Nitride) 박막의 전구물질로 이용하였으며, $70{\sim}120^{\circ}C$로 열을 가하여 열분해하였다. $25{\mu}m$ 두께의 구리 기판을 챔버에 넣어서 Low pressure (~25 mTorr) 상태가 되도록 한다. 25 mTorr 이하의 압력에서 수소 가스 (0.2~1sccm)를 넣고 $20^{\circ}C$/min로 가열한 후 약 한 시간 후에 $990{\sim}1,000^{\circ}C$가 된다. 그 후 Cu foil의 표면을 부드럽게 하고, 산화막을 제거하기 위해 $990^{\circ}C$에서 40 분간 열처리(annealing)한다. 그 후 암모니아 보레인에서 분해된 보라진 가스(borazine; B3H6N3)로 h-BN을 합성한다. 성장 시간이 길수록 더 많은 부분이 보론 나이트라이드에 의해 덮인다는 것을 관찰하였고, 성장 시 주입하는 수소의 양(0.2~5 sccm)과 알곤(0~15 sccm)의 혼합 비율에 따라 보론 나이트라이드의 domain size가 변화함을 알 수 있었다. 그 각각의 차이를 주사 전자현미경(SEM; Scanning Electron Microscopy)을 통해 확인하고, 결정성을 라만 분광(Raman spectroscopy), 광전자 분광(XPS; X-ray photoelectron spectroscopy)으로 비교 분석하였다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권23호
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• pp.10483-10487
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• 2015

Heptaphylline derivatives are carbazoles in Clausena harmandiana, a medicinal plant that is utilized for headache, stomach ache, and other treatments of illness. The present study examined the effects of heptaphylline and 7-methoxyheptaphylline on apoptosis of human colon adenocarcinoma cells (HT-29 cell line). Quantification of cell viability was performed using cell proliferation assay (MTT assay) and of protein expression through immunoblotting. The results showed that only heptaphylline, but not 7-methoxyheptaphylline, significantly significantly activated cleaved of caspase-3 and poly (ADP-ribose) polymerase (PARP-1) which resulted in HT-29 cell death. We found that heptaphylline activated BH3 interacting-domain death agonist (Bid) and Bak, proapoptotic proteins. In contrast, it suppressed X-linked inhibitor-of-apoptosis protein (XIAP), Bcl-xL and survivin, inhibitors of apoptosis. In addition, heptaphylline inhibited activation of NF-${\kappa}B$/p65 (rel), a regulator of apoptotic regulating proteins by suppressing the activation of Akt and $IKK{\alpha}$, upstream regulators of p65. The findings suggested that heptaphylline induces apoptosis in human colon adenocarcinoma cells.

• 한국미생물·생명공학회지
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• 제38권2호
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• pp.117-123
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• 2010

BT toxin is produced by a soil bacterium Bacillus thuringiensis and has long been used as a biological insecticide without any competition. Recently, Photorhabdus, a symbiotic bacterium from entomopathogenic nematodes, family Heterorhabditae, has been researched and discussed as alternatives to B. thuringiensis. Photorhabdus, which lives in the gut of entomopathogenic nematodes, is a highly virulent pathogen of a wide range of insect larvae. When an insect is infected by the nematodes, the bacteria are released into the cadaver, and produce a number of insecticidal toxins. The biological role of the different Photorhabdus toxins in the infection process is still unclear. Photorhabdus toxin complex (Tc) is highly secreted gut-active toxin and has been characterized as a potent three-component (A, B and C) insecticidal protein complex. These components are necessary for full oral activity against insect larvae. The Photorhabdus PirAB binary toxins exhibit a potent injectable activity for Galleria mellonella larvae, and have oral toxicity against mosquitoes and caterpillar pest Plutella xylostella. Other toxin, 'makes caterpillars floppy' (Mcf) showed injectable activity on caterpillars. Recombinant Mcf triggers apoptosis in both insect hemocytes and the midgut epithelium and carries a BH3 domain. In this review, the relationship between the Photorhabdus and the nematode is discussed and recent important insecticidal toxins from Photorhabdus are described.

• Asian Pacific Journal of Cancer Prevention
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• 제17권7호
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• pp.3131-3138
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• 2016

Several studies have addressed the possible role of hepatitis C virus genotype-4 (HCV GT4) in apoptosis. However, this still not fully understood. In the current study a re-constructed clone of E1/E2 polyprotein region of the HCV GT4 was transfected into the Huh7 cell line and a human apoptotic PCR array of 84 genes was used to investigate its possible significance for apoptosis. Out of the 84 genes, only 35 showed significant differential expression, 12 genes being up-regulated and 23 down-regulated. The highest-up regulated genes were APAF1 (apoptotic peptidase-activating factor 1), BID (BH3 interacting domain death agonist) and BCL 10 (B-cell CLL/lymphoma protein 10) with fold regulation of 33.2, 30.1 and 18.9, respectively. The most down-regulated were FAS (TNF receptor super family), TNFRSF10B (tumor necrosis factor receptor super-family member 10b) and FADD (FAS-associated death domain) with fold regulation of -30.2, -27.7 and -14.9, respectively. These results suggest that the E1/E2 proteins may be involved in HCV-induced pathogenesis by modulating apoptosis through the induction of the intrinsic apoptosis pathway and disruption of the BCL2 gene family.

• Molecules and Cells
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• 제37권3호
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• pp.264-269
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• 2014

The molecular interaction between tumor suppressor p53 and the anti-apoptotic Bcl-2 family proteins plays an essential role in the transcription-independent apoptotic pathway of p53. In this study, we investigated the binding of p53 DNA-binding domain (p53DBD) with the anti-apoptotic Bcl-2 family proteins, Bcl-w, Mcl-1, and Bcl-2, using GST pull-down assay and NMR spectroscopy. The GST pull-down assays and NMR experiments demonstrated the direct binding of the p53DBD with Bcl-w, Mcl-1, and Bcl-2. Further, NMR chemical shift perturbation data showed that Bcl-w and Mcl-1 bind to the positively charged DNA-binding surface of p53DBD. Noticeably, the refined structural models of the complexes between p53DBD and Bcl-w, Mcl-1, and Bcl-2 showed that the binding mode of p53DBD is highly conserved among the anti-apoptotic Bcl-2 family proteins. Furthermore, the chemical shift perturbations on Bcl-w, Mcl-1, and Bcl-2 induced by p53DBD binding occurred not only at the p53DBD-binding acidic region but also at the BH3 peptide-binding pocket, which suggests an allosteric conformational change similar to that observed in Bcl-$X_L$. Taken altogether, our results revealed a structural basis for a conserved binding mechanism between p53DBD and the anti-apoptotic Bcl-2 family proteins, which shed light on to the molecular understanding of the transcription-independent apoptosis pathway of p53.

• Asian Pacific Journal of Cancer Prevention
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• 제17권5호
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• pp.2637-2641
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• 2016

Tumor necrosis factor ($TNF-{\alpha}$), an inflammatory cytokine that plays an important role in the control of cell proliferation, differentiation, and apoptosis, has previously been used in anti-cancer therapy. However, the therapeutic applications of $TNF-{\alpha}$ are largely limited due to its general toxicity and anti-apoptotic influence. To overcome this problem, the present study focused on the effect of active constituents isolated from a medicinal plant on $TNF-{\alpha}$-induced apoptosis in human colon adenocarcinoma (HT-29) cells. Nimbolide from Azadirachta indica was evaluated for cytotoxicity by methyl tetrazolium 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay and phase contrast microscopy. Effects on apoptotic signaling proteins were investigated using Western blot analysis. Nimbolide showed cytotoxicity against HT-29 cells that was significantly different from the control group (p<0.01), a concentration of $10{\mu}M$ significantly inducing cell death (p<0.01). In combination with $TNF-{\alpha}$, nimbolide significantly enhanced-induced cell death. In apoptotic pathway, nimbolide activated c-Jun N-terminal kinase (JNK) phosphorylation, BH3 interacting-domain death agonist (Bid) and up-regulated the death receptor 5 (DR5) level. In the combination group, nimbolide markedly sensitized $TNF-{\alpha}$-induced JNK, Bid, caspase-3 activation and the up-regulation of DR5. Our findings overall indicate that nimbolide may enhance $TNF-{\alpha}$-mediated cellular proliferation inhibition through increasing cell apoptosis of HT-29 cells by up-reglation of DR5 expression via the JNK pathway.