• 생명과학회지
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• 제12권1호
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• pp.8-15
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• 2002

동결된 오리 MDM을 $25^{\circ}C$에서 약 3시간 방치하여 반해동시킨 후 얇게 자르고, 저온의 알칼리액(0.2% NaHCO$_3$와 0.15% NaCl 혼합액)으로 4시간 침지.교반하면서 수세처리한 후 다시 염지액 중에서 4시간 동안 교반하며 염지하였다. 염지가 끝난 육을 수세한 후 수분 80%이하로 탈수하여 silent cutter에 넣고 육만을 10분간 1차 고기갈이하고, 다시 식염을 첨가하여 30분간 2차 고기갈이를 하였다. 나머지 부원료와 첨가물, 즉 0.3% 폴리믹스 GA, 0.3% 폴리믹스 CS, 0.3% 피로인산염, 0.3% 중합인산염, 4.2% 설탕, 8% 전분, 7% 대두분리단백, 0.2% MSG, 0.5% 양파분말, 0.1% 마늘분말, 1.5% 넛멕, 0.1%이하의 솔빈산칼륨, 0.0075% 식용색소 적색 40호 7% 난백, gluten 3% 및 돈지 10%를 넣고 15분간 3차 고기갈이한 후 즉시 PVDC 필름에 공기가 들어가지 않게 충진하여 밀봉한 다음 9$0^{\circ}C$의 증기를 이용하여 80분간 가열하고 실온까지 급냉시켜 오리 MDM 소시지를 제조하였다.

• 한국해양공학회지
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• 제31권3호
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• pp.219-226
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• 2017

In this study, the impact characteristics of subsea pipelines that were installed in various soil types and burial depths were evaluated by a numerical method. An impact scenario replicated a dropped ship anchor that fell vertically and impacted an installed subsea pipeline. In order to calculate the impact force through terminal velocity, FLUENT, a computational fluid dynamic program and MDM (Moving Deforming Mesh) technique were applied. Next, a dynamic finite element program, ANSYS Explicit Dynamics, was used for impact analysis between the anchor and pipeline (or, subsea if they were buried). Three soil types were considered: loose sand, dense sand and soft clay by applying the Mohr-coulomb model to the seabed. The buried depth was assumed to be 0 m, 1 m and 2 m. In conclusion, a subsea pipeline was the most stable when buried in dense sand at a depth of 2 m to prevent impact damage.

• 생명과학회지
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• 제30권1호
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• pp.106-112
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• 2020

아미노아실-트랜스퍼 리보핵산 합성효소-상호작용 다기능 단백질 2(AIMP2)는 여러 tRNA 합성효소들과의 결합체를 이루게 하는 기능을 하며, DNA 손상에 대한 반응으로 세포사멸 활성을 나타낼 수 있다. DNA에 손상이 발생하면 AIMP2는 MDM2 공격으로부터 p53을 보호하기 위해 MDM2에 결합한다. TGF-β 신호에서 AIMP2는 세포 핵으로 들어가 FUSE 결합 단백질(FBP)과 결합하여 c-myc을 억제한다. TNF 수용체 관련 인자 2(TRAF2)는 c-Jun N-말단 키나아제(JNK), NF-κB 및 p38 미토겐 활성화 단백질 키나아제(MAPKs)의 신호에서 실행되는 두 수용체, TNF 수용체 1과 2 사이의 중요한 중재자이다. TARF2는 TNF-α 신호에서 JNK와 NF-κB의 활성화에 필요하며, 세포사멸 신호를 막는 중재자 역할을 수행한다. 또한 TNF-α 신호에서 AIMP2는 세포사멸을 향상시킨다. 이 신호에서, AIMP2는 TRAF2를 분해하는 것으로 잘 알려진 E3 유비키틴 효소인 c-IAP1과의 결합을 향상시킨다. AIMP2, TRAF2 및 c-IAP1을 포함한 복합체의 형성은 proteasome을 매개로 하여 TRAF2의 분해를 초래한다. 이러한 연구 결과는 AIMP2가 TNF-α 신호에서 직접적인 상호작용을 통해 TRAF2를 하향 조절시켜 세포사멸을 유도할 수 있음을 시사한다.

• BMB Reports
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• 제49권11호
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• pp.598-606
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• 2016

ARF is an alternative reading frame product of the INK4a/ARF locus, inactivated in numerous human cancers. ARF is a key regulator of cellular senescence, an irreversible cell growth arrest that suppresses tumor cell growth. It functions by sequestering MDM2 (a p53 E3 ligase) in the nucleolus, thus activating p53. Besides MDM2, ARF has numerous other interacting partners that induce either cellular senescence or apoptosis in a p53-independent manner. This further complicates the dynamics of the ARF network. Expression of ARF is frequently disrupted in human cancers, mainly due to epigenetic and transcriptional regulation. Vigorous studies on various transcription factors that either positively or negatively regulate ARF transcription have been carried out. However, recent focus on posttranslational modifications, particularly ubiquitination, indicates wider dynamic controls of ARF than previously known. In this review, we discuss the role and dynamic regulation of ARF in senescence and cancer.

• 천문학회보
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• 제42권1호
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• pp.50.2-50.2
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• 2017

We have been carrying out the long-term (3-5 years) AGN monitoring project since October 2015 to investigate the variability and measure the H beta line time lag of 69 nearby (0.06 < z < 0.47) AGNs based on the reverberation mapping method. Our targets have B band magnitudes of 14.4-18.6, luminosities of log L5100 = 45.6-48.1 erg/s, and the expected time lags of 28-597 light days. BVR band images are being taken with ~20-day cadence using MDM 1.3m, LOAO 1m and MDM 2.4m telescopes. Recently, Nickel 1m at Lick and DOAO 1m at Deokheung observatory are joined with photometric observations. Follow-up spectroscopic observations are on-going using the Lick 3m and MDM 2.4m telescopes. In this poster, we will describe our project including sample selection and the observational strategy, and present the preliminary results based on the 1st year photometry.

• Asian Pacific Journal of Cancer Prevention
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• 제14권3호
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• pp.1925-1929
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• 2013

Background: As a negative regulator of P53, MDM2 plays an important role in carcinogenesis; a polymorphism in its promoter region. SNP309 T>G, is known to increase the expression of MDM2, thus being considered related to higher susceptibility to neoplasia. However, no agreement has been achieved regarding its effects on gastric cancer. Methods: The present systematic meta-analysis was performed based on comprehensive literature search from Pubmed, Web of science and CBM databases. Results: It was suggested from 6 independent studies that the GG genotype is associated with a significantly increased risk of gastric cancer (Recessive: OR = 1.43, 95% CI = 1.08-1.91, P = 0.013), and subgroup analysis also confirmed the relationship (English publications-recessive model: OR = 1.45, 95% CI = 1.10-1.91, P = 0.009; Studies in China-recessive model: OR = 1.58, 95% CI = 1.08-2.30, P = 0.017). No publication bias was detected. Conclusion: The meta-analysis indicated a significant inverse association between GG genotype carriage and elevated risk of gastric cancer. However, more studies and detailed information are needed to fully address the topic.

• Toxicological Research
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• 제20권1호
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• pp.71-82
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• 2004

Changes in cell cycle control in the lungs and liver of the B6C3F1 mice (20 males per each group) exposed to ozone (0.5 ppm), 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK, 1.0 mg/kg), and dibutyl phthalate (DBP, 5,000 ppm) after 52 weeks were examined through Western, Northern blot, and immunohistochemistry based on alterations in protein expression levels of G1/S checkpoints (cyclin D1, cyclin E, and PCNA), G2/M checkpoints (cyclin B1, cyclin G, and cyclin A), negative regulators (p53, p21, GADD45, and p27), and positive regulator (mdm2). Expression levels of cyclins D1, E, G, PCNA, mutant p53, and mdm2 proteins were higher in the lungs and livers treated with combination of toxicants than in those treated with ozone only. Expression levels of the wild-type and mutant p53, p21, GADD45, p27, and mdm2 proteins and mRNAs were higher in toxicant-treated groups than those of the control. Immunohistochemical analysis revealed staining intensities of the PCNA, cyclin D1, c-myc and mdm2 protein- treated lungs and livers were stronger than those of the control group. Our results showed that combined treatment of ozone with NNK/DBP altered the cell cycle control through instability of the wild-type p53 gene. Such pivotal p53-mediated cell cycle alterations may be responsible for the toxicity observed under our experimental condition. These results may be applied to risk assessment of mixture-induced toxicity.

• 생명과학회지
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• 제19권4호
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• pp.436-441
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• 2009

B23/nucleophosmin은 핵인 단백질로서 외부 스트레스에 의해 핵인에서 핵으로 이동하게 된다. 이러한 세포 내 위치변화는 MDM2에 의한 p53단백질의 안정화에 영향을 미친다. 노화세포는 거대한 단일 핵인을 가지고 있으며, 외부 스트레스에 의해 p53 안정성이 감소한다. 그렇지만, 노화세포에서 어떠한 기전에 의해 p53의 불안정성이 증가하는 지는 아직 밝혀진 바가 없다. 따라서 본 연구에서는 노화세포에서 B23/nucleophosmin과 p53간의 상호 관련성을 조사하여 p53 안정성에 미치는 영향을 규명하고자 하였다. 본 연구에서는 IMR90세포주에 ras oncogene을 과발현시켜 노화세포를 유도하였다. 핵인 스트레스에 의해 노화세포 내 p53 단백질 발현은 감소하였으나, B23/nucleophosmin 단백질의 발현은 정상세포와 큰 차이가 없었다. 그렇지만, 두 단백질의 세포 내 위치는 노화세포에서 변화가 있었다. 즉, 정상세포와 달리, 노화세포에서는 스트레스에 의해 핵 내 p53발현이 증가하지 않았으며, B23/nucleophosmin은 핵 내로 이동하지 않고, 핵인에 그대로 머물러 있었다. 노화세포에서 MDM2와 p53간 상호결합이 안정적으로 유지된대 비하여, p53과 B23/nucleophosmin간의 상호결합은 감소하였다. 이러한 결과는 노화세포에서 핵인 스트레스에 의한 p53단백질의 안정성은 B23/nucleophosmin 결합이 감소하여 일어나는 것으로 해석된다.

• Animal cells and systems
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• 제16권3호
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• pp.173-182
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• 2012

The p53 protein plays a pivotal role in tumor suppression. The cellular level of p53 is normally kept low by proteasome-mediated degradation, allowing cell cycle progression and cell proliferation. Under stress conditions, such as DNA damage, p53 is stabilized and activated through various post-translational modifications of itself as well as of its regulatory proteins for induction of the downstream genes responsible for cell cycle arrest, DNA repair, and apoptosis. Therefore, the level of p53 should be tightly regulated for normal cell growth and for prevention of the accumulation of mutations in DNA under stress conditions, which otherwise would lead to tumorigenesis. Since the discovery of Mdm2, a critical ubiquitin E3 ligase that destabilizes p53 in mammalian cells, nearly 20 different E3 ligases have been identified and shown to function in the control of stability, nuclear export, translocation to chromatin or nuclear foci, and oligomerization of p53. So far, a large number of excellent reviews have been published on the control of p53 function in various aspects. Therefore, this review will focus only on mammalian ubiquitin E3 ligases that mediate proteasome-dependent degradation of p53.

• The Korean Journal of Physiology and Pharmacology
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• 제14권6호
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• pp.365-369
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• 2010

In this study, we examined whether melatonin promotes apoptotic cell death via p53 in prostate LNCaP cells. Melatonin treatment significantly curtailed the growth of LNCaP cells in a dose- and time-dependent manner. Melatonin treatment (0 to 3 mM) induced the fragmentation of poly(ADP-ribose) polymerase (PARP) and activation of caspase-3, caspase-8, and caspase-9. Moreover, melatonin markedly activated Bax expression and decreased Bcl-2 expression in dose increments. To investigate p53 and p21 expression, LNCaP cells were treated with 0 to 3 mM melatonin. Melatonin increased the expressions of p53, p21, and p27. Treatment with mitogen-activated protein kinase (MAPK) inhibitors, PD98059 (ERK inhibitor), SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor), confirmed that the melatonin-induced apoptosis was p21-dependent, but ERK-independent. With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease. These effects were opposite to the expression of p-p53, p21, and MDM2 observed with SP600125 and SB202190 treatments. Together, these results suggest that p53-dependent induction of JNK/p38 MAPK directly participates in apoptosis induced by melatonin.