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消費者의 衣服購買時 品質表示 制度의 認識度와 表示內容의 實態調査
殷英子,柳德桓,咸玉相 啓明大學校 生活科學硏究所 1988 科學論集 Vol.14 No.-
The purpose of this study was to investigate the purchasing pattern toward the garment's label and to find the problem of content's label. The questionnair method was used to obtained the data which was made by a result of self-administered questionnair, the lot of random sample for this paper was 390 subgects and the problem in the content's label was contemplate as the results of chemical method. The results indicate that; 1. The young's class, high scholarship and the small income earners had the more interest on the ready made clothes than the case of the contrary. 2. The group of 40∼50 year's old had the most interest in the garment label and the second case was the large income earner's and high scholarship's group. 3. An item of the interest in the label was the price and the size, everyone had understood generally the label contents, especially group of young's years all more than old year's, and the mark of Korean standard a little more than international standard's. 4. Percentages of the fibre blending were incorrected, especially mark's term was out of keeping by reason of the a bombastic advertisment.
Methylation of UHRF1 by SET7 is essential for DNA double-strand break repair
Hahm, Ja Young,Kim, Ji-Young,Park, Jin Woo,Kang, Joo-Young,Kim, Kee-Beom,Kim, Se-Ryeon,Cho, Hana,Seo, Sang-Beom Oxford University Press 2019 Nucleic acids research Vol.47 No.1
<P><B>Abstract</B></P><P>Ubiquitin-like with PHD and RING finger domains 1 (UHRF1) is a key epigenetic regulator of DNA methylation maintenance and heterochromatin formation. The roles of UHRF1 in DNA damage repair also have been emphasized in recent years. However, the regulatory mechanism of UHRF1 remains elusive. In this study, we showed that UHRF1 is methylated by SET7 and demethylation is catalyzed by LSD1. In addition, methylation of UHRF1 is induced in response to DNA damage and its phosphorylation in S phase is a prerequisite for interaction with SET7. Furthermore, UHRF1 methylation catalyzes the conjugation of polyubiquitin chains to PCNA and promotes homologous recombination for DNA repair. SET7-mediated UHRF1 methylation is also shown to be essential for cell viability against DNA damage. Our data revealed the regulatory mechanism underlying the UHRF1 methylation status by SET7 and LSD1 in double-strand break repair pathway.</P>
8-Oxoguanine: from oxidative damage to epigenetic and epitranscriptional modification
Hahm Ja Young,Park Jongyeun,Jang Eun-Sook,Chi Sung Wook 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
In pathophysiology, reactive oxygen species control diverse cellular phenotypes by oxidizing biomolecules. Among these, the guanine base in nucleic acids is the most vulnerable to producing 8-oxoguanine, which can pair with adenine. Because of this feature, 8-oxoguanine in DNA (8-oxo-dG) induces a G > T (C > A) mutation in cancers, which can be deleterious and thus actively repaired by DNA repair pathways. 8-Oxoguanine in RNA (o8G) causes problems in aberrant quality and translational fidelity, thereby it is subjected to the RNA decay pathway. In addition to oxidative damage, 8-oxo-dG serves as an epigenetic modification that affects transcriptional regulatory elements and other epigenetic modifications. With the ability of o8G•A in base pairing, o8G alters structural and functional RNA–RNA interactions, enabling redirection of posttranscriptional regulation. Here, we address the production, regulation, and function of 8-oxo-dG and o8G under oxidative stress. Primarily, we focus on the epigenetic and epitranscriptional roles of 8-oxoguanine, which highlights the significance of oxidative modification in redox-mediated control of gene expression.
Methylated-UHRF1 and PARP1 interaction is critical for homologous recombination
( Ja Young Hahm ),( Joo-young Kang ),( Jin Woo Park ),( Hyeonsoo Jung ),( Sang-beom Seo ) 생화학분자생물학회 2020 BMB Reports Vol.53 No.2
A recent study suggested that methylation of ubiquitin-like with PHD and RING finger domain 1 (UHRF1) is regulated by SET7 and lysine-specific histone demethylase 1A (LSD1) and is essential for homologous recombination (HR). The study demonstrated that SET7-mediated methylation of UHRF1 promotes polyubiquitination of proliferating cell nuclear antigen (PCNA), inducing HR. However, studies on mediators that interact with and recruit UHRF1 to damaged lesions are needed to elucidate the mechanism of UHRF1 methylationinduced HR. Here, we identified that poly [ADP-ribose] polymerase 1 (PARP1) interacts with damage-induced methylated UHRF1 specifically and mediates UHRF1 to induce HR progression. Furthermore, cooperation of UHRF1-PARP1 is essential for cell viability, suggesting the importance of the interaction of UHRF1-PARP1 for damage tolerance in response to damage. Our data revealed that PARP1 mediates the HR mechanism, which is regulated by UHRF1 methylation. The data also indicated the significant role of PARP1 as a mediator of UHRF1 methylation-correlated HR pathway. [BMB Reports 2020; 53(2): 112-117]
Depression in patients with SLE and their association with serum BDNF levels
( Sung Hae Chang ),( Ja Hyun Cho ),( Na Hee Shin ),( Hye Jin Oh ),( Myoung Jae Yoon ),( Eun Young Lee ),( Eun Bong Lee ),( Tae Jin Lee ),( Bong Jin Hahm ),( Young Wook Song ) 대한내과학회 2013 대한내과학회 추계학술발표논문집 Vol.2013 No.1
Introduction: Patients with systemic lupus erythematosus (SLE) are vulnerable to depression because of the chronic nature and neuropsychiatric involvement of the disease. Serum brain-derived neurotrophic factor (BDNF) was reported to be decreased in depression. The aim of the study was to investigate the prevalence of depression and its related factors including BDNF in patients with SLE. Material and Methods: One hundred and eighty patients were enrolled at the Rheumatology Clinic from January to March in 2012. The prevalence of depression was assessed using the center for epidemiologic studies depression (CES-D) scale. We evaluated disease activity by physician`s global assessment (PhyGA), patient`s global assessment (PGA), SLE disease activity index (SLEDAI) and disease related organ damage. The EuroQol-5 dimensions (EQ-5D), sociodemographic features and laboratory tests were also surveyed. Serum BDNF was measured using enzyme-linked immunosorbent assay (ELISA). Patients having a CES-D score of 24 or more were considered to have depression. Results: The prevalence of depression in SLE was 22.8% (n=41). In univariate analysis, unmarried/disrupted marital status (patients with single/divorced/estrangement/bereavement status than those with married status), unemployment, low annual income, higher PGA, higher PhyGA, lower EQ-5D index score and severe pain/discomfort were significantly associated with depression. In multivariate analysis, unmarried/disrupted marital status, higher PGA and severe pain/discomfort were significantly associated with depression. Serum BDNF levels were not associated with depression (p=0.62) but negatively correlated with disease activity in patients with SLE (r=-0.188, p=0.021). Conclusion: Depression is prevalent in patients with SLE and is associated with unmarried/disrupted marital status, severe pain/discomfort and higher PGA. Serum levels of BDNF were not associated with depression but were negatively correlated with disease activity. Treatment of depression may be beneficial in patients with severe pain/discomfort or high PGA.
Depression and Quality of Life in Patients with Systemic Lupus Erythematosus
( Sung Hae Chang ),( Ja Hyun Cho ),( Na Hee Shin ),( Hye Jin Oh ),( Byoong Yong Choi ),( Myeong Jae Yoon ),( Eun Young Lee ),( Eun Bong Lee ),( Yun Jong Lee ),( Tae Jin Lee ),( Bong Jin Hahm ),( Young 대한류마티스학회 2015 대한류마티스학회지 Vol.22 No.6
Objective. The objective of this study is to examine the prevalence of depression and its related factors including quality of life, brain-derived neurotrophic factor (BDNF), and vitamin D in patients with systemic lupus erythematosus (SLE). Methods. Depression was assessed using the center for epidemiologic studies depression (CES-D) scale. Disease activity, disease-related organ damage, the EuroQol-5 dimensions (EQ-5D), sociodemographic features, and laboratory tests including serum vitamin D level were surveyed. Serum BDNF was measured using an enzyme-linked immunosorbent assay. Results. Depression was observed in 22.8% of 180 SLE patients (n=41). Patients with marital status of single/divorced/separated/widowed, a higher patient global assessment (PGA) score, and extreme pain/discomfort showed significant association with depression. The EQ-5D index showed negative correlation with CES-D score (r=-0.56, p<0.05). In each EQ-5D dimension, depression showed significant association with moderate to severe problems in self-care and usual activities, and extreme pain/discomfort. Serum BDNF levels were not associated with depression (p=0.75) but associated with SLE disease activity index (SLEDAI; r=-0.21, p<0.05). Serum vitamin D levels were not associated with depression (p=0.60) but showed negative correlation with SLEDAI (r=-0.23, p<0.05) and mean glucocorticoid dose over the previous 3 months (r=-0.21, p<0.05) after adjustment for use of vitamin D supplement. Conclusion. Depression was prevalent in patients with SLE and was associated with low quality of life, and a higher PGA but not with SLEDAI. Serum BDNF and vitamin D levels were not associated with depression but showed negative correlation with SLEDAI. (J Rheum Dis 2015;22:346-355)
Regulation of UHRF1 acetylation by TIP60 is important for colon cancer cell proliferation
Hong Ye Joo,Park Junyoung,Hahm Ja Young,Kim Song Hyun,Lee Dong Ho,Park Kwon-Sik,Seo Sang-Beom 한국유전학회 2022 Genes & Genomics Vol.44 No.11
Background: Ubiquitin-like with PHD and RING finger domains 1 (UHRF1) is upregulated in colon cancer cells and associated with silencing tumor suppressor genes (TSGs) to promote colon cancer cell proliferation. Objective: To investigate epigenetic modification of UHRF1 by TIP60. Whether UHRF1 acetylation by TIP60 can induce cell proliferation in colon cancer cells. Methods: Acetylation sites of UHRF1 by TIP60 was predicted by ASEB (Acetylation Set Enrichment Based) method and identified by immunoprecipitation assay using anti-pan-acetyl lysine antibody and in vitro acetylation assay. Based on this method, UHRF1 acetylation-deficient mimic 4KR (K644R, K646R, K648R, K650R) mutant was generated to investigate effects of UHRF1 acetylation by TIP60. shRNA system was used to generate stable knockdown cell line of UHRF1. With transient transfection of UHRF1 WT and 4KR, the effects of UHRF1 4KR mutant on Jun dimerization protein 2 (JDP2) gene expression, cell proliferation and cell cycle were investigated by RT-qPCR and FACS analysis in shUHRF1 colon cancer cell line. Results: Downregulation of TIP60-mediated UHRF1 acetylation is correlated with suppressed cell cycle progression. Acetylation-deficient mimic of UHRF1 showed poor cell growth through increased expression of JDP2 gene. Conclusions: Acetylation of UHRF1 4K residues by TIP60 is important for colon cancer cell growth. Furthermore, upregulated JDP2 expression by acetylation-deficient mutant of UHRF1 might be an important epigenetic target for colon cancer cell proliferation.
Kim, Kee-Beom,Son, Hye-Ju,Choi, Sulji,Hahm, Ja Young,Jung, Hyeonsoo,Baek, Hee Jo,Kook, Hoon,Hahn, Yoonsoo,Kook, Hyun,Seo, Sang-Beom Oxford University Press 2015 Nucleic acids research Vol.43 No.7
<P>Histone H3K9 methyltransferase (HMTase) G9a-mediated transcriptional repression is a major epigenetic silencing mechanism. UHRF1 (ubiquitin-like with PHD and ring finger domains 1) binds to hemimethylated DNA and plays an essential role in the maintenance of DNA methylation. Here, we provide evidence that UHRF1 is transcriptionally downregulated by H3K9 HMTase G9a. We found that increased expression of G9a along with transcription factor YY1 specifically represses UHRF1 transcription during TPA-mediated leukemia cell differentiation. Using ChIP analysis, we found that <I>UHRF1</I> was among the transcriptionally silenced genes during leukemia cell differentiation. Using a DNA methylation profiling array, we discovered that the <I>UHRF1</I> promoter was hypomethylated in samples from leukemia patients, further supporting its overexpression and oncogenic activity. Finally, we showed that G9a regulates UHRF1-mediated H3K23 ubiquitination and proper DNA replication maintenance. Therefore, we propose that H3K9 HMTase G9a is a specific epigenetic regulator of UHRF1.</P>