• Proceedings of the Korea Crystallographic Association Conference
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• 2003.05a
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• pp.16-16
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• 2003

Mismatches in a DNA duplex are mainly due to DNA duplication errors that are generated by improper function of DNA polymerase. MutS, MutL and MutH are crucial proteins for the initiation of the methyl-directed mismatch repairing in bacteria. MutS has an ATPase activity md recognize the mismatched or unpaired bases on DNA. After binding to a mismatch, MutS recruits MutL to mediate the activation of MutH an endonuclease, which cleaves the 5' site of d(GATC) on the un-methylated strand. Both MutL and MutS also have essential roles in the subsequent removal and re-synthesis of the daughter strand. We have determined the crystal structures of either intact or active fragments of each of these proteins, both alone and complexed with ligands (DNA, ADP and ATP). The biochemical and mutagenesis studies based on the detailed 3-D structures led to new insights into the role of the ATPase activity of MutS in the mismatch recognition and directions for future investigation of mismatch repair.

• 한국전산유체공학회:학술대회논문집
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• 2008.08a
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• pp.32.2-32.2
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• 2008

• Journal of the Korean Society for Nondestructive Testing
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• v.24 no.6
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• pp.581-589
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• 2004

In this study, the capacitive micromachined ultrasonic transducer(cMUT) was developed based on the previous research results. The cross sectional image of the developed cMUT was characterized. To measure the membrane displacement of the cMUT, the Michelson phase modulation fiber interferometer was constructed. The measured membrane displacement was in good agreement with the result of the finite element analysis. To estimate the ultrasonic wave generated by the cMUT, an ultrasonic system including a pulser, receiver and charge amplifier was used. The cMUT developed in this study shows a good performance and hence will be widely used in the non-contact ultrasonic applications.

• 한국전산유체공학회:학술대회논문집
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• 2008.08a
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• pp.43.1-43.1
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• 2008

• The Journal of the Acoustical Society of Korea
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• v.39 no.2
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• pp.87-97
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• 2020

In this paper, the design of piezoelectric Micro-machined Ultrasonic Transducer (pMUT) for wideband ultrasonic radiation in air was investigated. One of the methods to achieve wide frequency bandwidth in single device is modeling the transducer to multi-resonance system. The new pMUT was designed as a multi-resonance system with the addition of a suitable acoustic structure to the front and back of a thin film structure. A new pMUT consisting of thin film parts, radiation parts, and packaging parts is designed with a Lumped Parameter Model (L.P.M). Finally, it was validated as a Finite Element Method (FEM) simulation. The final designed pMUT achieved a frequency band of 102 kHz ~ 132 kHz (-3 dB).

• BMB Reports
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• v.42 no.1
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• pp.53-58
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• 2009

The methyl-directed mismatch repair (MMR) mechanism has been extensively studied in vitro and in vivo, but one of the difficulties in determining the biological relationships between the MMR-related proteins is the tendency of MutL to self-aggregate. The properties of a stable MutL homologue were investigated using a thermostable MutL (TmL) from Thermotoga maritima MSB8 and whose size exclusion chromatographic and crosslinking analyses were compatible with a dimeric form of TmL. TmL underwent conformational changes in the presence of nucleotides and single-stranded DNA (ssDNA) with ATP binding not requiring ssDNA binding activity of TmL, while ADPnP-stimulated TmL showed a high ssDNA binding affinity. Finally, TmL interacted with the T. maritima MutS (TmS), increasing the affinity of TmS to mismatched DNA base pairs and suggesting that the role of TmL in the formation of a mismatched DNA-TmS complex may be a pivotal observation for the study of the initial MMR system.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.14 no.2
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• pp.174-177
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• 2014

Isolated methylmalonic acidemia (MMA) is a group of autosomal recessive inborn errors of metabolism caused by impaired activity of methylmalonyl-coenzyme A mutase (MCM). Mutations in the gene encoding MCM (MUT ) is the most common cause of isolated MMA. In this report, we identify an asymptomatic 15 days old female who had elevated C3-acylcarnitine (C3) in the newborn screening. Her serum homocysteine was normal and urine methylmalonic acid was increased that suggested isolated MMA. She was maintained on a low-protein diet and carnitine supplementation. At 3 months of age, she was still asymptomatic and had normal growth. We analyzed MUT gene mutations. Two heterozygote mutations in the MUT gene were identified including c.323G>A and c.1672+2T>C (IVS8(+2)T>C. Among these, c.1672+2T>C (IVS8(+2)T>C) have not been described previously.

• Journal of Life Science
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• v.26 no.7
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• pp.826-834
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• 2016

The present investigation was undertaken to examine the effectiveness of the combination treatment of an Hsp90 inhibitor and a SIRT1 inhibitor on suppressing the growth of chemo-resistant human cancer cells. We showed that inhibition of SIRT1 effectively potentiated the cytotoxicity of 17-allylamino-17-demethoxygeldanamycin (17-AAG) and reversed Hsp90 inhibitor resistance in multidrug-resistant (MDR) human ovarian HeyA8-MDR cells. Amurensin G, a potent natural SIRT1 inhibitor, enhanced Hsp90 inhibitor-mediated abrogation of the Hsp90 chaperone function and accelerated degradation of mutated p53 (mut p53), an Hsp90 client protein, by up-regulation of ubiquitin ligase CHIP. Knock-down of CHIP significantly attenuated amurensin G-induced mut p53 degradation. Down-regulation of mut p53 reduced the expression of heat shock factor1 (HSF1)/heat shock proteins (Hsps), a major cause of Hsp90 inhibitor resistance, which led to sensitization of the MDR cells to the Hsp90 inhibitor by the SIRT1 inhibitor. Amurensin G potentiated cytotoxicity of the Hsp90 inhibitor in HeyA8-MDR cells through suppression of 17-AAG-induced Hsp70 and Hsp27 induction via down-regulation of mut p53/HSF1, and it caused activation of PARP and inhibition of Bcl-2. Our data suggests that SIRT1 inhibitors could be used to sensitize MDR cells to Hsp90 inhibitors, possibly through suppression of the mut p53/HSF1-dependent pathway, and a novel mut p53-directed action of SIRT1 inhibition could effectively prevent mut p53 accumulation in MDR cells.

• Journal of the Korean Society for Nondestructive Testing
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• v.24 no.5
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• pp.487-493
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• 2004

This study was conducted to develope a capacitive micromachined ultrasonic transducer (cMUT) which enable to high efficient non-contact transmit and receive the ultrasonic wave in air. Theoretical analysis and finite element analysis of the behavior of membrane (such as resonance frequency, membrane deflection, collapse deflection and collapse voltage) of the cMUT were performed. The design parameters of the cMUT such as the dimension and thickness of membrane, thickness of sacrificial layer, thickness and size of electrode were estimated. The resonance frequency of the membrane increased as the thickness of the membrane increased but decreased as the diameter of the membrane increased. The deflection of the membrane increased as d-c bias voltage increased. The collapse voltage of the membrane was analyzed.

• 한국전산유체공학회:학술대회논문집
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• 2008.08a
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• pp.37.4-37.4
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• 2008