• 한국가금학회지
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• 제49권4호
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• pp.265-272
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• 2022

Many studies on poultry have been conducted in the poultry industry to improve their important economic traits, such as egg production, meat quality, and carcass yield. Environmental changes affect the poultry's economic traits, including muscle growth. The purpose of this study is to investigate the mechanisms by which simvastatin causes muscle injury in quail muscle cells. Following treatment with various doses of simvastatin, LD50 in the quail myoblast cells was determined using a cell viability test; cell death was caused by apoptosis and/or necrosis. Thereafter, the expression patterns of the atrophy marker genes were examined via quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The results showed that the transcriptional levels of the muscle atrophy marker genes (Atrogin-1, TRIM63) and the upstream genes in their signaling cascade were increased by simvastatin treatment. This indicated that simvastatin induced myogenic cell death and muscle injury via protein degradation through muscle atrophy signaling. Further studies should focus on identifying the mechanism by which simvastatin induces the protein degradation signaling pathway in quail muscle..

• 약학회지
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• 제51권5호
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• pp.350-354
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• 2007

Taurine has been shown to be tissue-protective against oxidant-induced injury and is a powerful regulator of the immune system. However, there is no study on the antimelanogenic effect of taurine. In this study, we investigated the whitening effect of taurine in B16F10 mouse melanoma cells. Cell viability was measured by MTT assay. We examined melanin contents and tyrosinase activity according to time and concentration. Extracellular signal regulated kinase (ERK) is an important regulator of melanogenesis. It has been reported that activated ERK induced microphthalmia associated transcription factor (MITF) phosphorylation and its subsequent degradation and thus reduced melanin synthesis. In our B16F10 cell culture system, taurine led to decrease melanin contents by 21% at 48 hr. We then observed taurine effects on ERK-P, MITF and tyrosinase by Western blot. ERK was activated at 18 hr and 24 hr, whereas MITF reduced. We could not observe any differences in the levels of tyrosinase. These results suggested that taurine inhibited melanogenesis by ERK signal pathway via MITF degradation. We expect that taurine has potential skin whitening agents in cosmetics.

• 대한화학회지
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• 제65권1호
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• pp.9-14
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• 2021

이 연구에서는 1기압 298 K 기체 상태에서 페난트렌에 두 개의 OH 라디칼이 연쇄적으로 작용하여 페난트렌이 분해되는 반응 과정을 B3LYP/6-31G(d,p) 기저함수를 사용하여 DFT 계산을 수행하였다. 계산 결과 두 개의 OH 라디칼이 연쇄적으로 페난트렌에 작용하는 경우에도 phenanthren-9-ol 생성 반응이 phenanthren-1-ol 생성 반응보다 유리할 것으로 예측된다. 한편 OH 첨가와 H 추출 과정에 대한 우선성은 상온에서 OH 첨가 과정이 유리할 것으로 예측되었다.

• 대한화학회지
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• 제62권5호
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• pp.344-351
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• 2018

이 연구에서는 기체 상태 페난트렌, 페난트렌올, 페난트레닐 라디칼, 하이드록실 페난트렌 라디칼에 대한 IR 스펙트럼을 BLYP/6-311++G(d,p)법을 사용하여 얻었다. 이 스펙트럼들을 비교함으로써 ${\cdot}OH$에 의한 페난트렌의 분해 반응 경로를 동정하는데 IR 스펙트럼 측정이 유용하게 사용될 수 있음을 볼 수 있었다. IR 스펙트럼에서 H 원자 제거 과정은 CH의 out-of-plane 굽힘 진동 영역인 $650{\sim}850cm^{-1}$, ${\cdot}OH$ 첨가 과정은 CH 신축 및 굽힘 진동 영역에서 용이하게 확인 할 수 있음을 알 수 있었다. 또한 5종의 페난트렌-n-올 (n = 1, 2, 3, 4, 9) 모두에 대하여 얻어진 IR 스펙트럼 역시 여기에 주어졌다.

• Journal of Microbiology and Biotechnology
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• 제10권1호
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• pp.111-114
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• 2000

Streptomyces are widespread in nature and play a very important role in the biosynthesis as well as biodegradation of natural and unnatural aromatic compounds. Both qualitatively and quantitatively through TLC and UV spectrophotometric assays, it was observed that the thermophilic soil bacteria S. setonii (ATCC 39116), which can utilize a benzoate as a sole carbon and energy source in a minimal liquid culture, was not very sensitive to the benzoate concentation and to the culture conditions such as the pH and temperature. The in vitro conversion of a catechol to a cis, cis-muconic acid by a crude S. setonii lysate implies that the aromatic ring cleavage by S. setonii is initiated by a thermostable catechol-1,2-dioxygenase, the key enzyme in the ortho-cleavage pathway of aromatic compound biodegradation. Unlike non-degrading S. lividans, S.setonii was also highly resistant to other similar hazardous aromatic compounds, exhibiting almost no adverse effect on its growth in a complex liquid culture.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2000년도 추계학술발표대회 및 bio-venture fair
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• pp.489-492
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• 2000

The eventual goal of this study is to elucidate roles of plant terpenoids (e.g., cymene, limonene and others) as natural substrates in the cometabolic biodegradation of PCBs and to develop an effective PCB bioremediation technology. The aim of this study was to examine how plant terpenoids, as natural substrates or inducers would affect the biodegradation of PCB congeners. Various PCB degraders that could grow on biphenyl and several terpenoids were tested for their PCB degradation capabilities. The PCB congener degradation activities were first monitored through resting cell assay technique that could detect degradation products of the substrate. The congener removal was also confirmed by concommitant GC analysis. The PCB degraders, Pseudononas sp. P166 and Caynebacterium sp. T104 were found to grow on both biphenyl and terpenoids ((S)-(-) limonene, p-cymene and ${\alpha}-terpinene$) whereas Arthrobacter B1B could not grow on the terpenoids as a sole carbon source. The strain B1B grown on biphenyl showed a good degradation activity for 4,4'-dichlorobiphenyl (DCBp) while strains P166 and T104 gave about 25% of B1B activity. Induction of degradation by cymene, limonene and terpine was hardly detected by the resting cell assay technique. This appeared to be due to relatively lower induction effect of these terpenoids compared with biphenyl. However, a subsequent GC analysis showed that the congener could be removed up to 30% by the resting cells of T104 grown on the terpenoids. This indicates that terpenoids, widely distributed in nature, could be utilized as both growth and/or inducer substrate for PCB biodegradation.

• Journal of Microbiology and Biotechnology
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• 제21권3호
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• pp.252-255
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• 2011

Both Escherichia coli (E. coli) and Salmonella enterica serovar Typhimurium (S. Typhimurium) have a tdc operon that encodes enzymes involved in a metabolic pathway for the degradation of L-serine and L-threonine. However, S. Typhimurium does not have the tdcR gene, which is a positive regulator in E. coli. In the present study, transcriptional analysis revealed that tdcA expression in E. coli is higher under anaerobic than aerobic growth conditions, but the opposite is true in S. Typhimurium. Interestingly, a tdcR mutant strain of E. coli showed a similar expression pattern to that observed in S. Typhimurium and was also induced by anaerobic shock. These results suggest that the induction of tdcA expression by anaerobic conditions is observable when tdcA expression is low owing to the absence of TdcR.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.90.1-90.1
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• 2003

This study shows that sphingosine-1-phosphate (S1P) significantly inhibits melanin synthesis in a concentration-dependent manner, and that the activity of tyrosinase was also reduced in S1P-treated cells. In contrast, a specific extracellular signal-regulated protein kinase (ERK) pathway inhibitor, PD98059 increased tyrosinase activity and melanin production, and PD98059 restored the reduced tyrosinase activity and pigmentation induced by SIP. We also found that S1P induces the sustained activation of ERK and the subsequent degradation of microphthalmia-associated transcription factor (MITF), which plays a key role in melanogenesis. (omitted)

• Molecules and Cells
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• 제28권1호
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• pp.49-55
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• 2009

Hepatitis delta virus (HDV) infection causes fulminant hepatitis and liver cirrhosis. To elucidate the molecular mechanism of HDV pathogenesis, we examined the effects of HDV viral proteins, the small hepatitis delta antigen (SHDAg) and the large hepatitis delta antigen (LHDAg), on $NF-{\kappa}B$ signaling pathway. In this study, we demonstrated that $TNF-{\alpha}-induced$ $NF-{\kappa}B$ transcriptional activation was increased by LHDAg but not by SHDAg in both HEK293 and Huh7 cells. Furthermore, LHDAg promoted TRAF2-induced $NF-{\kappa}B$ activation. Using coimmunoprecipitation assays, we demonstrated that both SHDAg and LHDAg interacted with TRAF2 protein. We showed that isoprenylation of LHDAg was not required for the increase of $NF-{\kappa}B$ activity. We further showed that only LHDAg but not SHDAg increased the $TNF-{\alpha}-mediated$ nuclear translocation of p65. This was accomplished by activation of $I{\kappa}B_{\alpha}$ degradation by LHDAg. Finally, we demonstrated that LHDAg augmented the COX-2 expression level in Huh7 cells. These data suggest that LHDAg modulates $NF-{\kappa}B$ signaling pathway and may contribute to HDV pathogenesis.

• Journal of Plant Biotechnology
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• 제37권1호
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• pp.57-66
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• 2010

Programmed cell death systems are important for an active type of cell deaths. Among them, a type of programmed cell death, autophagy is activated in cancer cells in response to multiple stresses and has been demonstrated to promote tumor cell survival and drug resistance. Thus, in the area of cancer, over the time frame form around the 1940s to date, of the 155 small molecules, 73% are other than "synthetic", with 47% actually being either "natural products" or "directly derived therefrom". Autophagy has multiple physiological functions in multicellular organisms, including protein degradation and organelle turnover. Genes and proteins that constitute the basic machinery of the autophagic process were first identified in the yeast system and some of their mammalian orthologues have been characterized as well. Numerous oncogenes, including Akt1, Bcl-2, NF1, PDPK1, class I PI3K, PTEN, and Ras and oncosuppressors, inculuding Bec-1, Bif-1, DAPK-1, p53 and UVRAG suppress or promote the autophagy pathway. Regulation of autophagy in tumors is governed by similar principles of the normal cells, only in a much more complicated manner, given the frequently observed abnormal PI3K activation in cancer and the multitude of interactions between the PI3K/AKT/mTOR pathway and other cell signaling cascades, often also deregulated in tumor cells. Autophagy induction by some anticancer agents underlines the potential utility of its induction as a new cancer treatment modality of development for natural medicines.