• 한국안광학회지
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• 제12권2호
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• pp.79-86
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• 2007

본 연구는 mycoplasma가 오염된 배양 각막 상피세포에 anti-FAS and anti-FAS ligand antibody를 노출시킨 후 세포고사 메커니즘을 조사하기 위해 시행하였다. 배양각막 상피세포에 anti-FAS antibody 와 anti-FAS ligand antibody를 2일과 4일 동안 처리하여 주어진 기간 동안 배양하였다. 배양 중인 각막상피세포가 mycoplasma sp.에 의해 오염된 것이 밝혀졌다. mycoplasma removal agent(MRA)가 세포주로부터 세균을 제거하기 위해 이용되었다. MRA를 세포주에 첨가하여 1주일 동안 배양하였다. 그 후 각막상피 세포주는 MRA가 포함되지 않는 배양액에서 수세대 동안 배양되어 커버글라스에 계대배양하여 50-80% 채워졌을 때 MRA 제거여부를 확인하기 위한 검사 키트에 제공된 Hoechst staining을 이용하여 염색하였다. 세포고사 실험은 MRA 제거 전과 제거 후에 시행되었다. mycoplasma가 오염된 배양 각막상피세포에 대한 anti-FAS and anti-FAS ligand antibody의 영향을 알아보기 위해 Hoechst 33342 staining과 Annexin V-FITC and Propidium Iodide Staining을 이용하여 세포고사 유도를 확인하였다. 본 연구는 anti-FAS antibody가 배양각막 상피세포에서 시간과 농도에 비례하는 메커니즘으로 세포고사를 유도한다. mycoplasma가 오염된 세포주는 FAS 유도 세포고사의 민감성을 증가시키는 것으로 나타났다.

• Biomolecules & Therapeutics
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• 제7권1호
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• pp.22-28
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• 1999

Induction of apoptosis is considered to be the underlying mechanism that accounts for the efficiency of chemotherapeutic drugs. It has recently been proposed that doxorubicin (DOX) can induce apoptosis in human leukemic cells via the Fas/Fas Ligand (FasL) system. Comparison of Fas and FasL mRNA expression between drug- and anti-Fas antibody(Fas-Ab)- induced apoptosis was analyzed for examining the role of Fas/FasL system in the mediation of drug-induced apoptosis. After HL-60 cells were routinely cultured, MTT assay was performed for cytotoxicity test. Giemsa staining was carried out to monitor the apoptosis morphologically. By semiquantitative RT-PCR analysis, the expression of Fas and FasL at 4, 10, 24 hours was determined after DOX and Fas-Ab treatment. Dose-dependent cytotoxicity was induced by DOX-treatment, while Fas-Ab treatment showed the similar dose-dependent pattern but the cytotoxicity is not reached at LD$_{50}$ at 100 ng/ml concentration of Fas-Ab. In the 10ng/m1 DOX and 10ng/m1 Fas-Ab treated group, typical apoptotic cell morphology was shown such as fragmented nuclei and cell membrane budding in the Giemsa-stained slide. Fas mRNA expression was not changed significantly in the both groups. But, FasL mRNA expression was induced significantly at initial period of apoptosis. In this study, Fas/FasL interaction assumed to be involved in drug-induced apoptosis.s.

• Toxicological Research
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• 제18권2호
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• pp.183-190
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• 2002

The mechanism by which catechin-mediated cytotoxicity against tumor cells remains to be elusive. To elucidate the mechanical mights of anti-tumor effects, (-)epigallocatechin-gallate (EGCG) of catechin was applied to human prostate cancer DU 145 cells. Cell viability was measured by crystal violet staining. Cell lysates were wed to measure the catalytic activity of caspases by using fluorogenic peptide: Ac-DEVD-AMC for caspase-3 protease, Z-IETD-AFC for caspase-8 protease, Ac-LEHD-AFC for caspase-9 protease as substrates. The equal amounts of protein from cell lysate was separated on SDS-PAGE and analyzed by western blotting with anti-Fas antibody, anti-FasL antibody, anti-BCL2 antibody and anti-Bax antibody. (-)EGCG induced the death of DUl45 cells, which was revealed as apoptosis shown by DNA fragmentation. (-)EGCG induced the activation of caspase family cysteine proteases including caspase-3, -8 and -9 proteases in DU145 cells. Also, (-)EGCG increased the expression of Fas and Fas ligand (FasL) protein in DU145 colls. The expression level of BCL2 was decreased in (-)EGCG treated DU145 cells, whereas Bax protein was increased in a time-dependent manner. We suggest that (-)EGCG-induced apoptosis of DU145 cells is mediated by signaling pathway involving caspase family cysteine protease, mitochondrial BCL2-family protein and Fas/FasL.

• IMMUNE NETWORK
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• 제11권4호
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• pp.210-215
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• 2011

It is already known that high concentration of vitamin C induces apoptosis on tumor cells. However, there is no report regarding the function of vitamin C on the modulation of immune susceptibility of cancer. Therefore, we investigated whether vitamin C can modulate immune susceptibility of tumor cells, especially on the induction of Fas-mediated apoptosis. First, the optimal concentration of vitamin C, which cannot induce damages on tumor cells for 36 hrs. We found that 2 mM of vitamin C did not show harmful effect. In addition, the optimal concentration of agonistic anti-Fas Abs for 18 hrs was examined. As a result, 400 ng/ml of agonistic anti-Fas Abs did not induce apoptosis on tumor cells. Next, we tried to find the effect of 2 mM of vitamin C on the modulation of the susceptibility to agonistic anti-Fas Abs. When tumor cells were cultured with 400 ng/ml of agonistic anti-Fas Abs for 18 hrs, after pre-treatment with 2 mM of vitamin C for 24 hrs, viability of cells was decreased. Interestingly, we found that the expression of Fas (CD95) and MHC class I was increased by the treatment of vitamin C. Taken together, vitamin C increases the susceptibility of tumor cells to anti-Fas Abs and the expression of Fas (CD95) and MHC class I on tumor cells.

• Archives of Pharmacal Research
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• 제27권4호
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• pp.402-406
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• 2004

This research team found in previous studies, that the ginseng saponin metabolite IH901 induces apoptosis in HepG2 cells via a mitochondrial-mediated pathway, which resulted in the activation of caspase-9 and subsequently of caspase-3 and -8. Based on these results, the involvement of the Fas/Fas ligand (FasL) death-receptor pathway, in IH901-induced apoptosis in HepG2 cells, was investigated. Levels of Fas and the Fas ligand (FasL) mRNA or protein were not increased by IH901, rather they were decreased significantly at 18 h post treatment. Soluble FasL (sFasL) was detectable by immunoprecipitation analysis En the medium of HepG2 cells treated with IH901. Increased levels of sFasL were inversely correlated with the levels of FasL. Preincubation of HepG2 cells with antagonistic anti-Fas antibody showed little protective effect, if any, on IH901-induced cell death. At a $30{\mu}M$ (24 and 48 h) and $40{\mu}M$ (24 h) concentration of IH901, the cytotoxic effect of IH901 was less then $50\%$, anti-Fas antibody prevented IH901-induced cell death. However, at a $60{\mu}M$ (24 and 48 h) and $40{\mu}M$ (48 h) concentration of IH901, cell death rates were about $80\%$ or more and most of the chemopreventive and chemotherapeutic effects of IH901 were manifested. Blocking the Fas receptor did not influence IH901-induced cell death. These results indicate that the Fas/FasL system is engaged, but not required for IH901-induced cell death, at pharmacologically significant concentrations.

• 한국전자통신학회논문지
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• 제19권1호
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• pp.309-316
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• 2024

얼굴 인식 기술은 다양한 분야에서 활용되고 있지만, 이는 사진 스푸핑과 같은 위조 공격에 취약하다는 문제를 가지고 있다. 이를 극복하기 위한 여러 연구가 진행되고 있지만, 대부분은 멀티모달 카메라와 같은 특별한 장비를 장착하거나 고성능 환경에서 동작하는 것을 전제로 하고 있다. 본 연구는 얼굴 인식 위조 공격 문제를 해결하기 위해, 특별한 장비 없이 일반적인 웹캠에서 동작할 수 있는 LH-FAS v2를 제안한다. 제안된 방법에서는, 머리 자세 추정에는 FSA-Net을, 얼굴 식별에는 ArcFace를 활용하여 사진 스푸핑 여부를 판별한다. 실험을 위해, 사진 스푸핑 공격 비디오로 구성된 VD4PS 데이터셋을 제시하였으며, 이를 통해 LH-FAS v2의 균형 잡힌 정확도와 속도를 확인하였다. 본 방법은 향후 사진 스푸핑 방어에 효과적일 것으로 기대한다.

• 대한한방내과학회지
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• 제24권1호
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• pp.123-133
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• 2003

Objectives : This study was designed to investigate the effects of Chungganhaeju-tang on expression of alcohol metabolizing enzymes, cell viability and alcohol-induced apoptosis. Materials and Methods : For this study, the human hepatoma cell line HepG2 was used. HepG2 cells were treated with ethanol-or acetaldehyde, chungganhaeju-tang, anti-Fas neutralizing antibody and were investigated by using quantitative RT-PCR, MTT and Trypan blue exclusion assays. Results : The results are summarized as follows: 1. Quantitative RT-PCR analysis demonstrated that ethanol-or acetaldehyde-mediated increase of ALDH gene expression was not affected by Chungganhaeju-tang treatment. 2, Ethanol-or acetaldehyde-induced apoptosis was remarkably inhibited by Chungganhaeju-tang in a dose-dependent manner. 3, Ethanol-or acetaldehyde-induced apoptosis was significantly blocked by anti-FasL neutralizing antibody, suggesting apoptosis induced by alcohol might be mediated by FasL/Fas signaling pathway. Conclusions : Taken all together, these results indicate that the FasL/Fas signaling plays a critical role in alcohol-induced apoptosis and Chungganhaeju-tang increases viability of liver cells by suppression of the FasL/Fas-mediated apoptosis-signaling pathway.

• IMMUNE NETWORK
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• 제6권2호
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• pp.59-66
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• 2006

Background: CM1 (Centrocyte/-blast Marker I) defined by a mAb developed against concanavalin-A activated PBMC, is expressed specifically on a subpopulation of centroblasts and centrocytes of human germinal center (GC) B cells. Burkitt lymphoma (BL) is a tumor consisting of tumor cells with the characteristics of GC B cell. Previously we reported that CM1 ligation with anti-CM1 mAb induced apoptosis in Ramos $(IgM^{high})$ and Raji $(IgM^{low})$ cells. Methods & Results: In the present study, we observed that CM1 ligation with anti-CM1 mAb induced Fas ligand and Fas expression in Ramos cells, but not in Raji cells. Furthermore, anti-Fas blocking antibody, ZB4, blocked CM1-mediated apoptosis effectively in Ramos cells, but not in Raji cells. Increased mitochondrial membrane permeabilization, which was measured by $DiOC_6$, was observed only in Raji cells. In contrast to no significant change of Bax known as pro-apoptotic protein, anti-apoptotic protein Bcl-2 was significantly decreased in Raji cells. In addition, we observed that CM1 ligation increased release of mitochondrial cytochrome c and upregulated caspase-9 activity in Raji cells. Conclusion: These results suggest that apoptosis induced by CM1-ligation is mediated by Fas-Fas ligand interaction in Ramos cells, whereas apoptosis is mediated by down-regulation of Bcl-2 and subsequent decrease of mitochondrial membrane potential in Raji cells.

• Journal of Life Science
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• 제10권1호
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• pp.57-63
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• 2000

${\beta}$-catenin, which plays a critical role in both the cytoskeleton and in transcriptional regulation in variousadherent cell types, undergoes degradation during adherent cell apoptosis. Although ${\beta}$-catenin has been reported to be present in Jurkat T-acute lymphoblastic leukemia cells, the regulation of ${\beta}$-catenin in hematologic malignancies have not been examined. The data presented here demonstrate that treatment of the T cell leukemia Jurkat iwht the apoptosis inducer anti-Fas induced proteolytic cleavage of ${\beta}$-catenin. ${\beta}$-catenin was cleaved at both the N- and C-terminus after anti-Fas treatment. Cleavage of intact ${\beta}$-catenin was completely inhibited by caspase selective protease inhibitors. These data demonstrate that ${\beta}$ -catenin proteolysis is triggered by the cross-linking of the Fas receptor on Jurkat cells and subsequent activation of caspase protease. There was a clear accumulatio of the large proteolytic fragment in Jurkat cells treated with lactacystin of ALLM. These are potent inhibitors of proteasome and calpain. these results suggest that both the proteasome and clapain may recognize the large ${\beta}$-catenin fragment as a substrate fot further degradation and that these pathewasy may act downstream of scapase in response to Fas receptor activation. Therefore, we suggest that ${\beta}$-catenin may play a role in promoting Jurkat survival.

• 한국정보처리학회:학술대회논문집
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• 한국정보처리학회 2021년도 추계학술발표대회
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• pp.651-654
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• 2021

Face anti-spoofing (FAS) techniques play a significant role in the defense of facial recognition systems against spoofing attacks. Existing FAS methods achieve the great performance depending on annotated additional modalities. However, labeling these high-cost modalities need a lot of manpower, device resources and time. In this work, we proposed to use self-transforming modalities instead the annotated modalities. Three different modalities based on frequency domain and temporal domain are applied and analyzed. Intuitive visualization analysis shows the advantages of each modality. Comprehensive experiments in both the CNN-based and transformer-based architecture with various modalities combination demonstrate that self-transforming modalities improve the vanilla network a lot. The codes are available at https://github.com/chenmou0410/FAS-Challenge2021.