• Journal of Korean Neurosurgical Society
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• 제29권10호
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• pp.1283-1288
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• 2000

Objectives : The subcellular locations of Bad, Bid, Bax and Bcl-XL change during apoptosis and this change is important for the regulation of cell death. The purpose this study was to elucidate binding of Bad with Bcl-XL in vivo Methods : We mads Bad with Green Fluorescent Protein(GFP) using PCR method. We transfected and overexpressed GFP-Bad with or without Bcl-XL cotransfection in living COS-7 cell. Results : Bad and Bcl- XL bind one another in healthy living cells and this association controled mitochondrial docking. In the absence of Bad-XL, Bad was mainly cytosolic and partially bound to mitochondria. Upon coexpression of Bad and Bcl-XL, most of Bad translocated to mitochondria. These should suggest that Bad binds to the mitochondrial and cytoplasmic forms of Bcl-XL and Bad bound to cytoplasmic Bcl-XL translocates to mitochondria. These in vivo findings confirm that Bad make a complexes with Bcl- XL and cause mitochondrial translocation of Bad-Bcl-XL complex.

• The Korean Journal of Physiology and Pharmacology
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• 제6권5호
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• pp.235-239
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• 2002

It has been reported that lovastatin induced cell death and suppressed proliferation in various cell lines. In this study, we examined whether the cytotoxic effects of lovastatin could be prevented by Bcl-2 or $Bcl-_{XL}$ in C6 glial cells. Overexpression of human Bcl-2 or $Bcl-_{XL}$ prevented lovastatin $(25{\mu}M)-induced$ changes such as DNA fragmentation, chromatin condensation, disruption of cell membrane, and cleavage of poly (ADP-ribose) polymerase. Lovastatin-induced inhibition of cell proliferation was unaffected by Bcl-2 or $Bcl-_{XL}$ overexpression. These results suggest that Bcl-2 and $Bcl-_{XL}$ can prevent lovastatin-induced apoptosis in C6 glial cells, though the inhibition of proliferation remains unaffected by these proteins.

• 한국진공학회지
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• 제14권3호
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• pp.138-142
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• 2005

액상 x-선 소각산란법을 이용하여 단백질의 구조를 분석하였다. 사용한 단백질은 구조가 이미 알려진 Lysozyme과 $Bcl-XL(\vartriangle TM/\vartriangle loop)$ 그리고 $Bcl-XL(\vartriangle TM/\vartriangle loop))$에 자유롭게 움직이는 고리를 가진 $Bcl-XL(\vartriangleTM))$이다. Lysozyme와 $Bcl-XL(\vartriangle TM/\vartriangle loop)$에 대한 소각산란결과는 단백질 결정학으로부터 알려진 분자구조에서 얻은 이론적인 결과와 농도에 의한 차이정도를 제외하고는 잘 일치하였다. $Bcl-XL(\vartriangleTM))$의 경우는 단백질 결정산란 신호에서 볼 때 $Bcl-XL(\vartriangle TM/\vartriangle loop)$와 차이가 없는 것으로 알려져 있으나, 소각산란에서는 뚜렷한 차이를 나타내는 결과를 얻어 loop와 같이 쉽게 움직이는 부분을 가진 단백질을 연구하는 경우 소각산란의 장점을 확인할 수 있었다. 위 실험을 통하여 포항 가속기 연구소 4C1 빔라인의 성능은 적어도 해상도 $\sim2.2\;nm$까지 용액상의 단백질 구조를 분석할 수 있다는 것을 확인하였다.

• 대한한방부인과학회지
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• 제21권4호
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• pp.90-103
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• 2008

목적 : 본 연구는 현호색의 메탄올 추출물(Corydalis Tuber Extract:CTE)이 인간 유방암 세포인 MCF-7 세포의 자멸사에 미치는 영향을 알아보고자 하였다. 방법 : 현호색 메탄올 추출물로 인간유방암에서 유래된 MCF-7 세포를 처리하였다. CTE의 세포자멸사 유도 효과는 MTT, FACS, TUNEL, DNA laddering and immunoblot assay를 통하여 측정하였다. 결과: 본 연구에서 현호색 메탄올 추출물은 MCF-7 세포의 활성을 감소시켰다. CTE로 처리한 MCF-7 세포는 용량에 따라 세포 자멸사 과정이 증가했다. CTE에 노출하였을 때 Bcl-2와 $Bcl-_{XL}$의 발현을 억제하고, 미토콘드리아로부터 세포질로 cytochrome-c를 방출하며, caspase와 PARP의 절단을 유발하여 세포자멸사가 증가했다. 현호색 메탄올 추출물에 존재하는 성분중에서 coptisine이 세포 활성도를 효과적으로 감소시킨 것으로 사료된다. 결론: 실험결과 현호색 메탄올 추출물이 유방암의 임상 치료에 있어 가능성 있는 치료 방법이 될 수 있을 것으로 사료된다.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2003년도 추계학술대회
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• pp.185-185
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• 2003

• BMB Reports
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• 제45권8호
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• pp.464-469
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• 2012

Endothelial cells (ECs) apoptosis induced by oxidized low-density lipoprotein (ox-LDL) is thought to play a critical role in atherosclerosis. MicroRNAs (miRNAs) are a class of noncoding RNAs that posttranscriptionally regulate the expression of genes involved in diverse cell functions, including differentiation, growth, proliferation, and apoptosis. MiRNA let-7 family is known to be involved in the regulation of cell apoptosis. However, the function of let-7 in ox-LDL induced ECs apoptosis and atherosclerosis is still unknown. Here, we show that let-7c expression was markedly up-regulated in ox-LDL induced apoptotic human umbilical cord vein endothelial cells (HUVECs). Let-7c over-expression enhanced apoptosis in ECs whereas inhibition of let-7c could partly alleviate apoptotic cell death mediated by ox-LDL. Searching for how let-7c affected apoptosis, we discovered that antiapoptotic protein Bcl-xl was a direct target of let-7c in ECs. Our data suggest that let-7c contributes to endothelial apoptosis through suppression of Bcl-xl.

• 대한약학회:학술대회논문집
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• 대한약학회 2000년도 NEW STRATEGY FOR DRUG DEVELOPMENT IN POST-GENOMIC ERA(대한약학회)
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• pp.207.1-207.1
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• 2000

• Asian Pacific Journal of Cancer Prevention
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• 제16권5호
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• pp.2087-2092
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• 2015

Nowadays herbal-derived medicines are attracting attention as new sources of drugs with few side effects. Silibinin is a flavonoid compound with chemotheraputic effects on different cancers such as examples in the prostate, lung, colon and breast. In the present study, the cytotoxic effects of silibinin on MCF7 breast cancer cells were investigated. Apoptosis was determined by flow cytometry and the impact of silibinin on the expression of pivotal genes including Bak, P53, P21, BRCA1, BCL-X1 and ATM was analyzed. Treatment for 24h had a significant dose-dependent inhibitory effect on cell growth (p<0.05) with dose- and time- dependent induction of apoptosis (p<0.05). In addition, there were significant increases in BRCA1, ATM, Bak and Bcl-XL gene expression at the mRNA level with different concentrations of silibinin for 24 or 48 h (p<0.05). Taken together, the results suggest that silibinin inhibits the proliferation and induces apoptosis of MCF-7 cells by down-regulating Bak, P53, P21, BRCA1, BCL-Xl and thus may be considered as an effective adjuvant drug to produce a better chemopreventive response for the cancer therapy.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.185-185
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• 2003

In-vitro expanded CNS precursors provide a potentially unlimited source of dopamine (DA) neurons for the experimental treatment in Parkinson's disease. An efficient dopaminergic differentiation from CNS precursors in vitro is limited to mesencephalic precursors isolated from early embryonic ages (embryonic day 11.5 (E11.5)-E12.5).(omitted)

• 동의생리병리학회지
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• 제20권6호
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• pp.1548-1555
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• 2006

Bujeonghangam-tang(BHT) has been used as an anticancer agent in oriental medicine, but the mechanism by which it induces cell death in cancer cells is still unclear. To investigate cell death mechanism by BHT in cancer cells, the activities of apoptosis signaling pathway were tested in human neuroblastoma cell line LAN5. Viability of LAN5 cells was markedly decreased by treatment of the water extract of BHT in a dose-dependent manner. BHT induced cell death was confirmed as apoptosis characterized by chromatin condensation. We tested whether the water extract of BHT affects the anti-apoptotic protein such as Bcl-2 and Bcl-XL, and the pro-apoptotic protein such as Bax. Both Bcl-2 and Bcl-XL were gradually decreased but Bas was increased in a time-dependent manner after the addition of the water extract of BHT. Cleavage of Bid by activation of caspase-8 protease was also observed in LAN-5 cells by the treatment of the water extract of BHT. Taken together, these results suggest that the water extract of BHT exerts anti-cancer effects on human neuroblastoma LAN-5 cells by inducing the apoptotic death via down-regulation of anti-apoptotic proteins such as Bcl-2 and Bcl-XL, up-regulation of pro-apoptotic protein such as Bax, and activation of intrinsic caspase cascades.