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국내 Fabry disease 환자의 a-Galatosidase A 유전자 돌연변이 검색
박기범,최지혜,강윤성,김선미,정향민,문영준,이광호 中央大學校 基礎科學硏究所 2001 基礎科學硏究所 論文集 Vol.15 No.-
Fabry disease(FD) is an X-linked recessive lysosomal disorder caused by a deficiency of a-galactosidase A(a-Gal A), localized at Xq22. Besides onset of pain and paresthesias in the extremities, FD was diagnosed by absence of a-Gal A activity. In this experiment the a-Gal A activity of Korean FD patients was spectrometrically analysed using an artificial substate, 4-Mrthylumbellifery1-a-D-galactoside. As expected, no a-Gal A activity was detected in lymphocytes and lymphoblastoid cells from FD patients. To screen the mutation in their a-Gal A genes, we performed single strand conformation polymorphism(SSCP) and PCR-direct sequencing form seven a-Gal A exons. The nonsense mutation was identified both in classically affected hemyzygotes and a heterozygote. They showed the C to T transition at nucleotide number 11,002, resulting in a arginine-to-stop(R342X). This result will be applicable for pre- and neonatal detection of FD and to define the genotype/phenotype correlation.
방민정 ( Min Cheong Bang ),윤미영 ( Mi Young Yun ),송향희 ( Hyang Hee Song ),노영희 ( Young Hee Noh ),정광조 ( Kwang Jo Cheong ) 한국미용학회 2009 한국미용학회지 Vol.15 No.4
The purpose of this study is to investigate the antioxidant activities of SanDalWood oil by experimental methods. For this purpose, first, we put an emphasis on the control of enzymes of the antioxidant system in various changes inside the cell; these changes caused by the reactive oxygen species (ROS) which were brought about by the handling of Lipopolysaccharide(LPS) into the RAW264.5 cell line of the body each other. After that, we caused the acute oxidant symptom by the injection of 2,2`-azobis(2-aminopropane) dihydrochloride(AAPH) into the mouse` abdominal cavity, and then applied the aroma SDWD oil orally administration, and finally, we measured the resistance against the activated oxygen of the red blood cell membrane, MDA, SOD, and catalase.
Aspergillus nidulans 에서 유성분화를 하지 못하는 여러 NSD 돌연변이체의 특성
한동민,정성수,한갑훈,허향숙 한국유전학회 1998 Genes & Genomics Vol.20 No.4
Several NSD (never in sexual development) mutants including one newly identified were characterized. None of cleistothecia were ever formed in standard conditions. NSD219 never developed any kind of sexual cells in any conditions. NSD204, NSD205 and NSD113 developed, however, normal cleistothecia on the minimal or complete media containing 3% glucose as C source. Growth of most mutants was retarded in compare with that of wild type. Asexual sporulation of the mutants occurred earlier than that of wild type. The nsdA, nsdB and nsdD loci were linked on linkage group II, V and VI, respectively. A novel NSD mutant, NSD113, belonged to the first group of the mutants which started to develop asexual spores just after release from aeration block. The mutant gene was complemented with nsdA4 and nsdB5 but not nsdD19 indicating that it was an another allele of nsdD locus. The mutant allele was named as nsdD13 and was revealed to locate on linkage group VI.
Ser1778 of 53BP1 Plays a Role in DNA Double-strand Break Repairs
Jung-Hee Lee,Hyang-Min Cheong,Mi-Young Kang,Sang-Young Kim,Yoonsung Kang 대한생리학회-대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.5
53BP1 is an important genome stability regulator, which protects cells against double-strand breaks. Following DNA damage, 53BP1 is rapidly recruited to sites of DNA breakage, along with other DNA damage response proteins, including Ճ-H2AX, MDC1, and BRCA1. The recruitment of 53BP1 requires a tandem Tudor fold which associates with methylated histones H3 and H4. It has already been determined that the majority of DNA damage response proteins are phosphorylated by ATM and/or ATR after DNA damage, and then recruited to the break sites. 53BP1 is also phosphorylated at several sites, like other proteins after DNA damage, but this phosphorylation is not critically relevant to recruitment or repair processes. In this study, we evaluated the functions of phosphor-53BP1 and the role of the BRCT domain of 53BP1 in DNA repair. From our data, we were able to detect differences in the phosphorylation patterns in Ser25 and Ser1778 of 53BP1 after neocarzinostatin-induced DNA damage. Furthermore, the foci formation patterns in both phosphorylation sites of 53BP1 also evidenced sizeable differences following DNA damage. From our results, we concluded that each phosphoryaltion site of 53BP1 performs different roles, and Ser1778 is more important than Ser25 in the process of DNA repair.
Ser1778 of 53BP1 Plays a Role in DNA Double-strand Break Repairs
Lee, Jung-Hee,Cheong, Hyang-Min,Kang, Mi-Young,Kim, Sang-Young,Kang, Yoon-Sung The Korean Society of Pharmacology 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.5
53BP1 is an important genome stability regulator, which protects cells against double-strand breaks. Following DNA damage, 53BP1 is rapidly recruited to sites of DNA breakage, along with other DNA damage response proteins, including ${\gamma}$-H2AX, MDC1, and BRCA1. The recruitment of 53BP1 requires a tandem Tudor fold which associates with methylated histones H3 and H4. It has already been determined that the majority of DNA damage response proteins are phosphorylated by ATM and/or ATR after DNA damage, and then recruited to the break sites. 53BP1 is also phosphorylated at several sites, like other proteins after DNA damage, but this phosphorylation is not critically relevant to recruitment or repair processes. In this study, we evaluated the functions of phosphor-53BP1 and the role of the BRCT domain of 53BP1 in DNA repair. From our data, we were able to detect differences in the phosphorylation patterns in Ser25 and Ser1778 of 53BP1 after neocarzinostatin-induced DNA damage. Furthermore, the foci formation patterns in both phosphorylation sites of 53BP1 also evidenced sizeable differences following DNA damage. From our results, we concluded that each phosphoryaltion site of 53BP1 performs different roles, and Ser1778 is more important than Ser25 in the process of DNA repair.
( Han Heom Na ),( Hee Jung Noh ),( Hyang Min Cheong ),( Yoonsung Kang ),( Keun Cheol Kim ) 생화학분자생물학회(구 한국생화학분자생물학회) 2016 BMB Reports Vol.49 No.4
The efficacy of anticancer drugs depends on a variety of signaling pathways, which can be positively or negatively regulated. In this study, we show that SETDB1 HMTase is down-regulated at the transcriptional level by several anticancer drugs, due to its inherent instability. Using RNA sequence analysis, we identified FosB as being regulated by SETDB1 during anticancer drug therapy. FosB expression was increased by treatment with doxorubicin, taxol and siSETDB1. Moreover, FosB was associated with an increased rate of proliferation. Combinatory transfection of siFosB and siSETDB1 was slightly increased compared to transfection of siFosB. Furthermore, FosB was regulated by multiple kinase pathways. ChIP analysis showed that SETDB1 and H3K9me3 interact with a specific region of the FosB promoter. These results suggest that SETDB1- mediated FosB expression is a common molecular phenomenon, and might be a novel pathway responsible for the increase in cell proliferation that frequently occurs during anticancer drug therapy. [BMB Reports 2016; 49(4): 238-243]
경기도내에서 분리한 호흡기아데노바이러스의 혈청형 분포특성
이현경,이명진,문수경,김운호,조한길,윤미혜,이정복,정향민,Lee, Hyun-Kyung,Lee, Myung-Jin,Mun, Su-Kyoung,Kim, Woon-Ho,Cho, Han-Gil,Yoon, Mi-Hye,Lee, Jong-Bok,Cheong, Hyang-Min 한국미생물학회 2012 미생물학회지 Vol.48 No.3
아데노바이러스는 다양한 급성호흡기감염증을 유발하며, 대부분 영유아나 어린이, 면역기능이 저하된 환자에게서 주로 나타나는 것으로 알려져 있다. 본 연구에서는 2009년부터 2011년까지 경기지역 소아청소년과 및 내과에 내원한 급성호흡기 감염증 의심환자를 대상으로 호흡기아데노바이러스의 유행양상 및 혈청형 분포양상을 분석하였다. 총 1,622명의 급성상기도 감염증이 의심되는 환자의 검체를 분석한 결과 102건(6.3%)에서 아데노바이러스를 검출하였다. 102건의 아데노바이러스 양성 검체에서 세포배양법으로 76주의 아데노바이러스를 분리하였고, 혈청형별 특이유전자인 헥손 유전자의 염기서열 분석을 통하여 혈청형을 확인하였다. 최근 3년간 경기도내에서 아데노바이러스 1형부터 6형까지 6개의 다른 혈청형이 분리되었고, 이 중 3형(n=40, 52.6%)이 가장 주류를 이루었다. 2009년에는 1형과 3형, 2010년에는 3형, 2011년에는 5형이 각각 우점하였다. 1, 2, 4, 5, 6형은 연중 산발적으로 확인되었으나, 3형은 산발적으로 발생하면서 2010년에는 큰 유행을 일으킨 것을 확인할 수 있었다. 본 연구결과를 통해 최근 3년동안 경기도내 아데노바이러스에 의한 outbreak의 주 원인 혈청형은 아데노바이러스 3형임을 알 수 있었고, 앞으로도 outbreak의 원인이 되는 특정 혈청형에 대한 지속적인 감시가 이루어져야 할 것이다. Adenoviruses are an important cause of respiratory tract infections, particularly in infants, young children, and immuno-compromised patients. In this study, we investigated the characteristics of adenoviruses isolated from outpatients with acute respiratory illness in Gyeonggi province of South Korea during 2009-2011. Adenoviruses were detected in 102 of 1,622 (6.3%) specimens by using PCR or real-time PCR with viral specific primers. 76 isolates were obtained from 102 specimens using the A549 cells. Serotypic distributions of isolated adenovirus were analyzed by sequencing of hexon gene. Six different serotypes were identified, which included adenovirus serotypes 1-6. Adenovirus 3 (n=40, 52.6%) was the predominant serotype. The predominant types of adenovirus every year were serotypes 1 and 3 in 2009, serotype 3 in 2010, and serotype 5 in 2011, respectively. Adenoviruses 1, 2, 4, 5, and 6 were isolated sporadically throughout the study period. Adenovirus 3 was present both during outbreaks and in sporadic cases. These results indicate that adenovirus 3 played major causative agent of adenovirus outbreaks in Gyeonggi province of South Korea during 2009-2011. Continuous surveillance for specific serotypes of adenovirus that can cause outbreaks is important.