• Journal of Veterinary Science
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• v.21 no.3
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• pp.45.1-45.15
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• 2020

Background: Feline mammary carcinoma is the third most common cancer that affects female cats. Objectives: The purpose of this study was to screen differential serum proteins in feline and clarify the relationship between them and the occurrence of feline mammary carcinoma. Methods: Chinese pastoral cats were used as experimental animals. Six serum samples from cats with mammary carcinoma (group T) and six serum samples from healthy cats (group C) were selected. Differential protein analysis was performed using a Label-free technique, while parallel reaction monitoring (PRM) was performed to verify the screened differential proteins. Results: A total of 82 differential proteins were detected between group T and group C, of which 55 proteins were down regulated and 27 proteins were up regulated. Apolipoprotein A-I, Apolipoprotein A-II (ApoA-II), Apolipoprotein B (ApoB), Apolipoprotein C-III (ApoC-III), coagulation factor V, coagulation factor X, C1q, albumen (ALB) were all associated with the occurrence of feline mammary carcinoma. Differential proteins were involved in a total of 40 signaling pathways, among which the metabolic pathways associated with feline mammary carcinoma were the complement and coagulation cascade and cholesterol metabolism. According to the Label-free results, ApoB, ApoC-III, ApoA-II, FN1, an uncharacterized protein, and ALB were selected for PRM target verification. The results were consistent with the trend of the label-free. Conclusions: This experimen is the first to confirm ApoA-II and ApoB maybe new feline mammary carcinoma biomarkers and to analyze their mechanisms in the development of such carcinoma in feline.

• Clinical and Experimental Pediatrics
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• v.49 no.6
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• pp.617-622
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• 2006

Purpose : High-Sensitivity C-reactive protein(hs-CRP) has been recognized as a very useful and sensitive predictor of the future risk of myocardial infarction. But the clinical significance of hs-CRP in children remains uncertain. To confirm the existence of obesity-induced vascular inflammation and the association between metabolic syndromes and elevation of CRP in children, we investigated the relationship among CRP, obesity, blood pressure(BP), and serum lipids in schoolboys. Methods : Twenty-eight obese(BMI $29.61{\pm}3.29kg/m^2$) and 93 non-obese(BMI $18.99{\pm}2.21kg/m^2$) boys aged 14 years were examined. Serum CRP levels was measured by the high sensitive latex turbidimetric immunoassay and subjects with CRP levels below 0.3 mg/dL were adopted to avoid the influence of acute infection. Results : Obese children had significantly higher hs-CRP levels than their non-obese group($0.104{\pm}0.075$ vs. $0.054{\pm}0.005mg/dL$). In the obese group, BMI, systolic blood pressure, diastolic blood pressure, apolipoprotein B, atherogenic index, and triglyceride were significantly higher than in nonobese. The BMI, diastolic blood pressure, apolipoprotein E, atherognic index, and triglyceride showed positive correlation with log CRP by simple regression. Multiple regression analysis indicated that BMI and apolipoprotein E were strongly related to CRP. Conclusion : This study revealed that obese children tended to have higher levels of serum hsCRP, BP elevation and dyslipidemia than the control group and that BMI and apolipoprotein E were strongly related to CRP. These results indicate that obesity related metabolic syndrome can be developed in children.

• Biomedical Science Letters
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• v.11 no.4
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• pp.429-434
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• 2005

Apolipoprotein E (apoE) restriction isotyping used oligonucleotides to amplify apoE gene sequences containing amino acid positions 112 and 158. The amplification products were digested with HhaI and subjected to electrophoresis on $4\%$ agarose gel. Each of the isoforms was distinguished by a unique combination of HhaI fragment sizes that enabled unambiguous typing of all homozygotic and heterozygotic combinations. HhaI cleaves at GCGC encoding 112arg (E4) and 158arg (E3, E4), but does not cut at GTGC encoding 112cys (E2, E3) and] 58cys (E2). DNA was isolated from 72 study participants and apoE genotypes were determined utilizing the polymerase chain reaction and restriction isotyping. In the entire group of subjects, $38 (52.8\%)$ had apo E4/4 or E3/4 (Group E4), $28(38.9\%)$ had the apo E3/3 genotype (Group E3) and $6(8.3\%)$ had apo E2/2 or E2/3 (Group E2). This genotypic information may help to identify individuals at increased risk for several diseases.

• Environmental Mutagens and Carcinogens
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• v.22 no.4
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• pp.243-247
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• 2002

Prolonged exercise is known to increase steady-state serum high-density lipoprotein cholesterol (HDL-cholesterol) and apolipoprotein AI(apo AI) concentrations. We investigated the effect of adaptation to endurance exercise on the association of the genetic polymorphism in the apo AI gene with these biochemical parameters. 108 male subjects were randomly selected from a group of elite athletes, and 65 male samples used as sedentary control group from Korean general population. The genetic polymorphism in the apo AI gene locus was detected by polymerase chain reaction(PCR) and DNA digestion with Msp I restriction endonuclease. The genotype frequency for the Msp I RFLP was significantly different between the elite athletes and sedentary controls(P<0.05). There were, however, no significant associations between the Msp I RFLP of the apo AI gene and the biochemical parameters in elite athletic group. Therefore, our findings indicate that the Msp I RFLP of the apo AI gene was not associated with the serum apo AI and HDL-cholesterol concentrations in Korean male elite athletes.

• The Journal of Korean Medicine
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• v.24 no.4
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• pp.113-119
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• 2003

The association between apolipoprotein E (apo E) gene polymorphism and ischemic cerebrovascular disease (ICVD) has been controversial. These controversies may be due to inaccurate classification of patients and ethnic differences. We investigated the association between apo E genotypes and ICVD patients by case-control study in a Korean population. The association between apo E polymorphism and ICVD was examined in 121 patients with ICVD and 132 controls without ICVD. The E3/E4 phenotype was more frequent in control subjects (23.8％) than in patients (13.0％) (p<0.05). The E2/E3 phenotype was more frequent in patients (14.8％) than in control subjects (10.8％), but the difference was not statistically significant (p>0.05). These results suggest that the E4 allele may be a protective factor against early vascular morbidity, and the E2 allele may be a risk factor for cerebrovascular morbidity.

• Preventive Nutrition and Food Science
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• v.7 no.4
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• pp.353-357
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• 2002

We have previously demonstrated that kudzu root extracts have a hypocholesterolemic effect on rats fed diets high in fat and cholesterol. To further elucidate the mechanism involved, in this study we investigated the effect of water extracts of kudzu root, Pueraria radix, on the production of apolipoprotein B$_{100}$ (APo B$_{100}$) in HepG$_2$ liver cells and secretion of apolipoprotein B$_{48}$ (Apo B$_{48}$) in Caco$_2$ cells. Human cell lines, HepG$_2$ liver cells and Caco$_2$ intestinal epithelial cells, were grown with various concentrations (0%, 0.5%, 1.0%, 1.5%, 2.0%) of water extracts of kudzu root in the media. The kudzu root extract decreased Apo B$_{100}$ production and secretion. Treatment of HeP G$_2$ cells with the kudzu root extract also significantly decreased the intracellular total and free cholesterol concentration, and also decreased esterified cholesterol but was only significant at the highest dose of 2%. Apo B$_{48}$ production, but not secretion, from enterocytes was lowered by the kudzu root extracts. This research provided evidence that the hypocholesterolemic properties of kudzu root may be a consequence of decreased production and secretion of Apo B$_{100}$ in the liver and Apo B$_{48}$ in the intestine.

• Molecules and Cells
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• v.26 no.3
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• pp.291-298
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• 2008

Human karyopherin ${\beta}3$, highly homologous to a yeast protein secretion enhancer (PSE1), has often been reported to be associated with a mediator of a nucleocytoplasmic transport pathway. Previously, we showed that karyopherin ${\beta}3$ complemented the PSE1 and KAP123 double mutant. Our research suggested that karyopherin beta has an evolutionary function similar to that of yeast PSE1 and/or KAP 123. In this study, we performed yeast two-hybrid screening to find a protein which would interact with karyopherin ${\beta}3$ and identified apolipoprotein A-I (apo A-I), a secretion protein with a primary function in cholesterol transport. By using in vitro binding assay, co-immunoprecipitation, and colocalization studies, we defined an interaction between karyopherin ${\beta}3$ and apo A-I. In addition, overexpression of karyopherin ${\beta}3$ significantly increased apo A-I secretion. These results suggest that karyopherin ${\beta}3$ plays a crucial role in apo A-I secretion. These findings may be relevant to the study of a novel function of karyopherin ${\beta}3$ and coronary artery diseases associated with apo A-I.

• Journal of Ginseng Research
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• v.38 no.4
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• pp.251-255
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• 2014

Background: Ginsenoside Rp1 (G-Rp1) is a novel ginsenoside derived from ginsenoside Rk1. This compound was reported to have anticancer, anti-platelet, and anti-inflammatory activities. In this study, we examined the molecular target of the antiproliferative and proapoptotic activities of G-Rp1. Methods: To examine the effects of G-Rp1, cell proliferation assays, propidium iodine staining, proteomic analysis by two-dimensional gel electrophoresis, immunoblotting analysis, and a knockdown strategy were used. Results: G-Rp1 dose-dependently suppressed the proliferation of colorectal cancer LoVo cells and increased their apoptosis. G-Rp1 markedly upregulated the protein level of apolipoprotein (Apo)-A1 in LoVo, SNU-407, DLD-1, SNU-638, AGS, KPL-4, and SK-BR-3 cells. The knockdown of Apo-A1 by its small-interfering RNA increased the levels of cleaved poly(ADP-ribose) polymerase and p53 and diminished the proliferation of LoVo cells. Conclusion: These results suggest that G-Rp1 may act as an anticancer agent by strongly inhibiting cell proliferation and enhancing apoptosis through upregulation of Apo-A1.

• Bulletin of the Korean Chemical Society
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• v.25 no.12
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• pp.1845-1849
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• 2004

Apolipoprotein B-100 (Apo-B100) is a major protein component for low density lipoproteins (LDL). A number of mimetic peptides of Apo-B100 were screened from the phase-displayed random peptide library by utilizing monoclonal antibody (B9). Mimetic peptide for B9 epitope against apo B-100 was CRNVPPIFNDVYWIAF (pB1). From the BLAST search, the mimetic peptide pB1 had 40% homology with apo B-100. As a result of the structural determination of this mimotope using homo/hetero nuclear 2D-NMR techniques and NMR-based distance geometry (DG)/molecular dynamic (MD) computations, DG structure had low penalty value of 0.3-0.6 ${\AA}^2$ and the total RMSD was 0.5-1.5 ${\AA}. Moreover, pB1 structure included a weak $3_{10}$-helix from $Ile^7$,/TEX> to $Trp^{13}$.

• Molecules and Cells
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• v.42 no.11
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• pp.739-746
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• 2019

Significant knowledge about the pathophysiology of Alzheimer's disease (AD) has been gained in the last century; however, the understanding of its causes of onset remains limited. Late-onset AD is observed in about 95% of patients, and APOE4-encoding apolipoprotein E4 (ApoE4) is strongly associated with these cases. As an apolipoprotein, the function of ApoE in brain cholesterol transport has been extensively studied and widely appreciated. Development of new technologies such as human-induced pluripotent stem cells (hiPSCs) and CRISPR-Cas9 genome editing tools have enabled us to develop human brain model systems in vitro and readily manipulate genomic information. In the context of these advances, recent studies provide strong evidence that abnormal cholesterol metabolism by ApoE4 could be linked to AD-associated pathology. In this review, we discuss novel discoveries in brain cholesterol dysregulation by ApoE4. We further elaborate cell type-specific roles in cholesterol regulation of four major brain cell types, neurons, astrocytes, microglia, and oligodendrocytes, and how its dysregulation can be linked to AD pathology.