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Search Results: 1 - 10 of 26028 matches for " Eun Jeoung Lee "
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Tip60 Tumor Suppressor Requires Its NLS Motif to Interact with Importin α  [PDF]
Eun Jeoung Lee, Sung Hwa Shin, Sang Sun Kang
CellBio (CellBio) , 2019, DOI: 10.4236/cellbio.2019.81001
Abstract: Tip60 is a specific member of MYST (Moz-Ybf2/Sas3-Sas2-Tip60) family of nuclear histone acetyltransferases (HAT). It is essential for cellular survival, differentiation, and metabolism. A putative canonical NLS motif between the chromo domain and the zinc finger of Tip60 was identified. Here we show evidence that Tip60 is associated with importin α as its substrate and transported from cytoplasm to the nucleus. Pull down assay revealed that Tip60 was physically associated with importin α both in vivo and in vitro. Confocal microscopic observation showed that Tip60 and importin α were co-localized with each other. The localization of Tip60 to the nuclear and its interaction with importin α was disrupted when its putative NLS motif for binding to importin α was mutated (219RKRK222 219AAAA222). However, attachment of this putative NLS motif to a cytoplasmic protein (YAP 1-210 fragment) promoted its nuclear localization. Based on transient transfection, Tip60 NLS motif mutant showed a substantial reduction in self-acetylation, HAT activity, and apoptotic ability whereas wild type Tip60 did not show such reduction. Taken together, our results demonstrate that importin α transports Tip60 from the cytoplasm to the nucleus through binding to the putative NLS motif of Tip60 for its tumor suppressing function.
The interaction between Fe65 and Tip60 is regulated by S-nitrosylation on 440 cystein residue of Fe65  [PDF]
Eun Jeoung Lee, Sung Hwa Shin, Sunghee Hyun, Jaesun Chun, Sang Sun Kang
Advances in Biological Chemistry (ABC) , 2011, DOI: 10.4236/abc.2011.13013
Abstract: The S-Nitrosylation of protein thiol groups by NO is a widely recognized protein modification. The treat-ment of cells with NOBF4 induces the S-nitrosylation of FE65. In this study, we present evidence showing that FE65 modified by NO (Nitric Oxide) via S-nitrosylation induces functional changes in the protein that inhibits the HAT activity of Tip60. The results of mutational analysis of FE65 demonstrated further that the cysteine residue of FE65 (Cys440) is critical to the process of S-nitrosylation. The mutation of the cysteine residue which completely ablated the S-nitrosylation of FE65 also lost its inhibitory effects on Tip60 HAT activity. Thus, our findings show, for the first time, that the novel regulation mechanism of Tip60 activity may operate via FE65 binding, which is enhanced by S-nitrosylation on the FE65 Cys440 residue. This study describes the interaction between FE65 and Tip60, which is enhanced by a posttransla-tional modification of FE65 (through S-nitrosylation) by NO, promoting the association of the FE65-Tip60 protein complex and inhibiting both the HAT activity of Tip60 and cell death.
Phosphorylation on TRPV4 Serine Residue 824 Enhances Its Association with PGM1  [PDF]
Sung Hwa Shin, Eun Jeoung Lee, Sunghee Hyun, Sang Sun Kang
American Journal of Molecular Biology (AJMB) , 2016, DOI: 10.4236/ajmb.2016.61004
Abstract: The TRPV4 cation channel is expressed in a broad range of tissues and participates in the generation of a Ca2+ signal and/or depolarization of membrane potential. Here, human phosphoglucomutase- 1 (PGM1), an enzyme that converts glucose-6 phosphate to glucose-1 phosphate in the glycolysis pathway, as the first auxiliary protein of TRPV4 Ca2+ channels, is identified with yeast two hybrid system, coimmunoprecipitation, confocal microscopy, and GST pull-down assays. TRPV4 forms a complex with PGM1 through its C-terminal cytoplasmic domain. Because it is demonstrated that TRPV4 serine residue 824 (S824) is phosphorylated by serum/glucocorticoid regulated kinase 1, we elucidate the effect of TRPV4 S824 phosphorylation on TRPV association with PGM1. Even an inactivated mutant version of TRPV4, S824A, exhibited a decreased ability to bind PGM1, an activated phosphomimetic mutant version of TRPV4, S824D, exhibited enhanced binding to PGM1. Thus, formation of the TRPV4/PGM1 complex and localization of this complex to the plasma membrane appear to be regulated by the phosphorylation status of residue S824 in TRPV4. The newly identified interactor of TRPV4 may help the molecular pathways modulating transport activity or glucose metabolism, respectively.
Three-Step Method for Proliferation and Differentiation of Human Embryonic Stem Cell (hESC)-Derived Male Germ Cells
Jung Jin Lim, Myung Sun Shim, Jeoung Eun Lee, Dong Ryul Lee
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0090454
Abstract: The low efficiency of differentiation into male germ cell (GC)-like cells and haploid germ cells from human embryonic stem cells (hESCs) reflects the culture method employed in the two-dimensional (2D)-microenvironment. In this study, we applied a three-step media and calcium alginate-based 3D-culture system for enhancing the differentiation of hESCs into male germ stem cell (GSC)-like cells and haploid germ cells. In the first step, embryoid bodies (EBs) were derived from hESCs cultured in EB medium for 3 days and re-cultured for 4 additional days in EB medium with BMP4 and RA to specify GSC-like cells. In the second step, the resultant cells were cultured in GC-proliferation medium for 7 days. The GSC-like cells were then propagated after selection using GFR-α1 and were further cultured in GC-proliferation medium for 3 weeks. In the final step, a 3D-co-culture system using calcium alginate encapsulation and testicular somatic cells was applied to induce differentiation into haploid germ cells, and a culture containing approximately 3% male haploid germ cells was obtained after 2 weeks of culture. These results demonstrated that this culture system could be used to efficiently induce GSC-like cells in an EB population and to promote the differentiation of ESCs into haploid male germ cells.
Does the Duration and Time of Sleep Increase the Risk of Allergic Rhinitis? Results of the 6-Year Nationwide Korea Youth Risk Behavior Web-Based Survey
Jeoung A. Kwon, Minjee Lee, Ki-Bong Yoo, Eun-Cheol Park
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072507
Abstract: Allergic rhinitis (AR) is the most common chronic disorder in the pediatric population. Although several studies have investigated the correlation between AR and sleep-related issues, the association between the duration and time of sleep and AR has not been analyzed in long-term national data. This study investigated the relationship between sleep time and duration and AR risk in middle- and high-school students (adolescents aged 12–18). We analyzed national data from the Korea Youth Risk Behavior Web-based Survey by the Korea Centers for Disease Control and Prevention from 2007–2012. The sample size was 274,480, with an average response rate of 96.2%. Multivariate logistic regression analyses were conducted to determine the relationship between sleep and AR risk. Furthermore, to determine the best-fitted model among independent variables such as sleep duration, sleep time, and the combination of sleep duration and sleep time, we used Akaike Information Criteria (AIC) to compare models. A total of 43,337 boys and 41,665 girls reported a diagnosis of AR at baseline. The odds ratio increased with age and with higher education and economic status of the parents. Further, students in mid-sized and large cities had stronger relationships to AR than those in small cities. In both genders, AR was associated with depression and suicidal ideation. In the analysis of sleep duration and sleep time, the odds ratio increased in both genders when sleep duration was <7 hours, and when the time of sleep was later than 24:00 hours. Our results indicate an association between sleep time and duration and AR. This study is the first to focus on the relationship between sleep duration and time and AR in national survey data collected over 6 years.
Does Stress Increase the Risk of Atopic Dermatitis in Adolescents? Results of the Korea Youth Risk Behavior Web-Based Survey (KYRBWS-VI)
Jeoung A. Kwon, Eun-Cheol Park, Minjee Lee, Ki-Bong Yoo, Sohee Park
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067890
Abstract: This study investigated the relationship between level of stress in middle and high school students aged 12–18 and risk of atopic dermatitis. Data from the Sixth Korea Youth Risk Behavior Web-based Survey (KYRBWS-VI), a cross-sectional study among 74,980 students in 800 middle schools and high schools with a response rate of 97.7%, were analyzed. Ordinal logistic regression analyses were conducted to determine the relationship between stress and atopic dermatitis with severity. A total of 5,550 boys and 6,964 girls reported having been diagnosed with atopic dermatitis. Younger students were more likely to have atopic dermatitis. Interestingly, the educational level of parents was found to be associated with having atopic dermatitis and having more severe condition. In particular, girls with mothers with at least college education had a 41% higher risk of having atopic dermatitis and severe atopic condition (odds ratio (OR)) = 1.41, 95% CI, 1.22–1.63; P<0.0001) compared with those with mothers who had attended middle school at most. Similar trend was shown among both boys and girls for their father's education level. The stress level was found to be significantly associated with the risk of atopic dermatitis. Compared to boys with who reported “no stress”, boys with “very high” stress had 46% higher the risk of having more severe atopic dermatitis (OR = 1.46, 95% CI, 1.20–1.78; P<0.0001), 44% higher (OR = 1.44, 95% CI, 1.19–1.73; P<0.0001) with “high” stress, and 21% higher (OR = 1.21, 95% CI, 1.00–1.45; P = 0.05) with “moderate” stress. In contrast, we found no statistically significant relationship between stress and atopic dermatitis in girls. This study suggests that stress and parents' education level were associated with atopic dermatitis. Specifically, degree of stress is positively correlated with likelihood of being diagnosed with this condition and increasing the severity.
Embryonic Demise Caused by Targeted Disruption of a Cysteine Protease Dub-2
Kwang-Hyun Baek, Heyjin Lee, Sunmee Yang, Soo-Bin Lim, Wonwoo Lee, Jeoung Eun Lee, Jung-Jin Lim, Kisun Jun, Dong-Ryul Lee, Young Chung
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0044223
Abstract: Background A plethora of biological metabolisms are regulated by the mechanisms of ubiquitination, wherein this process is balanced with the action of deubiquitination system. Dub-2 is an IL-2-inducible, immediate-early gene that encodes a deubiquitinating enzyme with growth regulatory activity. DUB-2 presumably removes ubiquitin from ubiquitin-conjugated target proteins regulating ubiquitin-mediated proteolysis, but its specific target proteins are unknown yet. Methodology/Principal Findings To elucidate the functional role of Dub-2, we generated genetically modified mice by introducing neo cassette into the second exon of Dub-2 and then homologous recombination was done to completely abrogate the activity of DUB-2 proteins. We generated Dub-2+/? heterozygous mice showing a normal phenotype and are fertile, whereas new born mouse of Dub-2?/? homozygous alleles could not survive. In addition, Dub-2?/? embryo could not be seen between E6.5 and E12.5 stages. Furthermore, the number of embryos showing normal embryonic development for further stages is decreased in heterozygotes. Even embryonic stem cells from inner cell mass of Dub-2?/? embryos could not be established. Conclusions Our study suggests that the targeted disruption of Dub-2 may cause embryonic lethality during early gestation, possibly due to the failure of cell proliferation during hatching process.
Functional Integration of the Conserved Domains of Shoc2 Scaffold
Myoungkun Jeoung, Lina Abdelmoti, Eun Ryoung Jang, Craig W. Vander Kooi, Emilia Galperin
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0066067
Abstract: Shoc2 is a positive regulator of signaling to extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). Shoc2 is also proposed to interact with RAS and Raf-1 in order to accelerate ERK1/2 activity. To understand the mechanisms by which Shoc2 regulates ERK1/2 activation by the epidermal growth factor receptor (EGFR), we dissected the role of Shoc2 structural domains in binding to its signaling partners and its role in regulating ERK1/2 activity. Shoc2 is comprised of two main domains: the 21 leucine rich repeats (LRRs) core and the N-terminal non-LRR domain. We demonstrated that the N-terminal domain mediates Shoc2 binding to both M-Ras and Raf-1, while the C-terminal part of Shoc2 contains a late endosomal targeting motif. We found that M-Ras binding to Shoc2 is independent of its GTPase activity. While overexpression of Shoc2 did not change kinetics of ERK1/2 activity, both the N-terminal and the LRR-core domain were able to rescue ERK1/2 activity in cells depleted of Shoc2, suggesting that these Shoc2 domains are involved in modulating ERK1/2 activity.
An endomorphism of the Khovanov invariant
Eun Soo Lee
Mathematics , 2002,
Abstract: We construct an endomorphism of the Khovanov invariant to prove H-thinness and pairing phenomena of the invariants for alternating links. As a consequence, it follows that the Khovanov invariant of an oriented nonsplit alternating link is determined by its Jones polynomial, signature, and the linking numbers of its components.
The support of the Khovanov's invariants for alternating knots
Eun Soo Lee
Mathematics , 2002,
Abstract: In this article, we prove the conjecture of Bar-Natan, Garoufalidis, and Khovanov's on the support of the Khovanov's invariants for alternating knots.
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