• Journal of Life Science
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• v.12 no.1
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• pp.8-15
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• 2002

In this paper we dealt with processing of sausage using duck mechanically deboned meat(duck-MDM). The results may be summarized as follows : 1) after semi-thawing of freezing duck-MDM at $25^{\circ}C$ for 3 hours and cutting as thin, 2) alkali washing at low temperature for 4 hours by 0.2% NaHCO$_3$and 0.15% NaCl, 3) curing at low temperature for 4 hours, 4) after washing and dehydrating(moisture 80%), 5) grinding at low temperature for 55 minutes by silent cutter such as 1st grinding for 10 minutes added only dehydrated meat, 2rd grinding for 30 minutes added salt in 1st grinded meat and 3rd grinding for 15 minutes added other additives, 6) after quick casing in PVDC film and heating at 9$0^{\circ}C$ for 80 minutes, 7) cooling to below room temperature. The additives added at 3rd grinding process were Polymix-CA(0.3%), Polymix-CS(0.3%), polyphosphate(0.3%), sugar(4.2%), potato starch(8.0%), pyre-phosphates(0.3%), isolated soy protein(7.0%), MSG(0.2%), onion powder(0.5%), garlic powder(0.1%), nutmeg (1.5%), potassium sorbate(<0.1%), food red no.40(0.0075%), egg albumin(7.0%) and gluten(3.0%).

• Journal of Ocean Engineering and Technology
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• v.31 no.3
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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.

• Journal of Life Science
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• v.30 no.1
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• pp.106-112
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• 2020

Aminoacyl tRNA synthetase complex interacting multifunctional protein 2 (AIMP2) is a scaffolding protein required for the assembly of multi-tRNA synthetase, and it can exert pro-apoptotic activity in response to DNA damage. In the presence of DNA damage, AIMP2 binds to mouse double minute 2 homolog (MDM2) to protect p53 from MDM2 attack. TGF-β signaling results in the nuclear translocation of AIMP2, whereby AIMP2 interacts with FUSE-binding protein, and, thus, suppresses c-myc. TNF receptor-associated factor 2 (TRAF2) is an important mediator between TNF-receptors 1 and 2 which are involved in the signaling of c-Jun N-terminal kinase (JNK), nuclear factor κB (NF-κB), and p38 mitogen-activated protein kinases (MAPKs). TRAF2 is required for the activations of JNK and NF-κB via TNF-α and the mediation of anti-apoptosis signaling. AIMP2 can also enhance pro-apoptosis in the TNF-α signaling. During this signaling, AIMP2 assists the association of E3 ubiquitin ligase, the cellular inhibitor of apoptosis protein 1 (c-IAP1) which is well known and responsible for the degradation of TRAF2. The formation of a complex among AIMP2, TRAF2, and c-IAP1 results in proteasome-mediated TRAF2 degradation. AIMP2 can induce apoptosis via downregulation of TRAF2 to interact directly in TNF-α signaling. This review provides new insight into the molecular mechanism responsible for AIMP2 and TRAF2 complex formation and treatments for TNFα-associated diseases.

• BMB Reports
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• v.49 no.11
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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.

• The Bulletin of The Korean Astronomical Society
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• v.42 no.1
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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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• v.14 no.3
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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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• v.20 no.1
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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.

• Journal of Life Science
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• v.19 no.4
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• pp.436-441
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• 2009

B23/nucleophosmin, a nucleolar protein, translocates into the nucleus from the nucleolus when cells are damaged by extracellular stresses. Recently, it was shown that such translocation of B23/nucleophosmin in normal fibroblasts under stress conditions increases both the stability and activation of the p53 protein by disrupting its interaction with MDM2. Senescent cells have a single large nucleolus and a diminished capacity to induce p53 stability upon exposure to various DNA damaging agents. To investigate the role of B23/nucleophosmin in p53 stability in senescent cells, we established a senescence model system by expressing the ras oncogene in IMR90 cells. The stability of p53 was reduced in these cells in response to nucleolar stress, although the level of B23/nucleophosmin protein was not changed. In addition, p53 did not accumulate in the nucleus and B23/nucleophosmin did not translocate into the nucleoplasm. The binding affinity of B23/nucleophosmin with p53 was reduced in senescent cells, whereas the interaction between MDM2 and p53 was stable. Taken together, the stability of p53 in ras-induced senescent cells may be influenced by the ability of B23/nucleophosmin to interact with p53 in response to nucleolar stress.

• Animal cells and systems
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• v.16 no.3
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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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• v.14 no.6
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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.