• 제목/요약/키워드: Apo A1

검색결과 198건 처리시간 0.033초

Solution State Structure of pB1, the Mimotopic Peptide of Apolipoprotein B-100, by NMR

  • Lee, Sung-Ran;Kim, Dae-Sung;Kim, Hyo-Joon;Lee, Yong-Woo;Won, Ho-Shik
    • Bulletin of the Korean Chemical Society
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    • 제25권12호
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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 $Trp^{13}$.

Assessment of an Apo-1/Fas Promoter Polymorphism in Korean Schizophrenia Patients

  • Kim, Soon-Ae;Kim, Youn-Jung;Choe, Bong-Keun;Lee, Hee-Jae;Kim, Jong-Woo;Park, Jong-Deuk;Kim, Chang-Ju;Park, Seung-Joon;Jung, Jee-Chang;Chung, Joo-Ho
    • The Korean Journal of Physiology and Pharmacology
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    • 제6권3호
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    • pp.161-163
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    • 2002
  • Apoptosis has been hypothesized to be involved in the pathogenesis in schizophrenia. A large number of genes are known to mediate the apoptotic process; Apo-1/Fas (CD95) is a well-known example of such genes. In the present study, MvaI restriction fragment length polymorphism, a polymorphic marker present within the Apo-1/Fas gene, was examined in a population consisting of 226 control subjects and 110 schizophrenia patients, all of them Korean in ethnicity. No statistically significant difference in the genotypic distribution and allelic frequencies was observed between the control and the schizophrenia patient group. To find out the precise effect of Apo-1/Fas gene polymorphisms on the susceptibility to schizophrenia, further studies are warranted to investigate possible involvement of other polymorphisms with a larger sample population.

Korean pine nut oil replacement decreases intestinal lipid uptake while improves hepatic lipid metabolism in mice

  • Zhu, Shuang;Park, Soyoung;Lim, Yeseo;Shin, Sunhye;Han, Sung Nim
    • Nutrition Research and Practice
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    • 제10권5호
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    • pp.477-486
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    • 2016
  • BACKGROUND/OBJECTIVES: Consumption of pine nut oil (PNO) was shown to reduce weight gain and attenuate hepatic steatosis in mice fed a high-fat diet (HFD). The aim of this study was to examine the effects of PNO on both intestinal and hepatic lipid metabolism in mice fed control or HFD. MATERIALS/METHODS: Five-week-old C57BL/6 mice were fed control diets containing 10% energy fat from either Soybean Oil (SBO) or PNO, or HFD containing 15% energy fat from lard and 30% energy fat from SBO or PNO for 12 weeks. Expression of genes related to intestinal fatty acid (FA) uptake and channeling (Cd36, Fatp4, Acsl5, Acbp), intestinal chylomicron synthesis (Mtp, ApoB48, ApoA4), hepatic lipid uptake and channeling (Lrp1, Fatp5, Acsl1, Acbp), hepatic triacylglycerol (TAG) lipolysis and FA oxidation (Atgl, Cpt1a, Acadl, Ehhadh, Acaa1), as well as very low-density lipoprotein (VLDL) assembly (ApoB100) were determined by real-time PCR. RESULTS: In intestine, significantly lower Cd36 mRNA expression (P<0.05) and a tendency of lower ApoA4 mRNA levels (P = 0.07) was observed in PNO-fed mice, indicating that PNO consumption may decrease intestinal FA uptake and chylomicron assembly. PNO consumption tended to result in higher hepatic mRNA levels of Atgl (P = 0.08) and Cpt1a (P = 0.05). Significantly higher hepatic mRNA levels of Acadl and ApoB100 were detected in mice fed PNO diet (P<0.05). These results suggest that PNO could increase hepatic TAG metabolism; mitochondrial fatty acid oxidation and VLDL assembly. CONCLUSIONS: PNO replacement in the diet might function in prevention of excessive lipid uptake by intestine and improve hepatic lipid metabolism in both control diet and HFD fed mice.

Comparative study of linear and cyclic forms of apoptosis-targeting peptide

  • Ha, Yeong Su;Soni, Nisarg;Huynh, Phuong Tu;Lee, Byung-Heon;An, Gwang Il;Yoo, Jeongsoo
    • 대한방사성의약품학회지
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    • 제2권2호
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    • pp.96-102
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    • 2016
  • Apoptosis, a genetically determined process of programmed cell death, is considered a vital component of various processes including normal cell turnover, animal development, and tissue homeostasis. It has a crucial role in many medical disorders and hence the development of non-invasive imaging tool is highly demanded. Recently, we have developed a peptide-based radioactive probe (ApoPep-1) for apoptosis detection. In that work the potential of probe for apoptosis detection was verified, however in vivo stability of radiolabeled peptide was not enough to monitor apoptosis for extended period. In current study, we prepared cyclic ApoPep-1 peptides to improve the stability of origianl linear ApoPep-1 and carried out direct comparison studies in vitro and in vivo. A targeting efficacy of newly synthesized cyclic ApoPep-1 peptide for apoptosis was confirmed in acute myocardial infarct model.

한국인 직장성인과 그 배우자의 Aplipoprotein A-I & B 분포 (Apolipopretein A-I and B Distribution among the Employees and their Partners in Korea)

  • 김원술;김동일;서병성
    • Journal of Preventive Medicine and Public Health
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    • 제40권1호
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    • pp.71-76
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    • 2007
  • Objectives : This study was performed to investigate the distribution of apolipoproteins A-I and B among Korean employees and their partners. Methods : The study population consisted of 7,633 men and women (4,578 men and 3,054 women) residing in Seoul and Kyung-gee Do, with an average age of $43.5{\pm}8.3$ years. Blood samples were collected following at least 12 hours of fasting. Apolipoproteins A-I and B were measured using a Behring Nephelometer analyzer. The body mass index (BMI) for each participant was calculated as weight (kg) divided by height squared $(m^2)$. Information on health-related behaviors such as exercise, alcohol intake, and smoking habits was collected through self-administrated questionnaires. Results : The mean concentrations of Apo A-I were $132.6{\pm}22.3mg/dL$ and $142.9{\pm}24.8mg/dL$ in the men and women, respectively. The concentration of Apo A-I increased significantly across all age categories of men. The mean concentrations of Apo B were $101.7{\pm}23.2mg/dL$ and $87.8{\pm}23.5mg/dL$ in the men and women, respectively, and Apo B increased significantly across all age categories for both the men and women. Exercise and BMI were major determinants for Apo A-I and B levels. The 10th percentile of Apo A-I concentration was 109 mg/dL in the men and 113 mg/dL in the women, and the 90th percentile of Apo B concentration was 131 mg/dL in the men and 118 mg/dL women. Conclusions : For the prevention of coronary artery disease, we recommend that for individuals in the 10th percentile of concentration for Apo A-I and the 90th percentile of concentration for Apo B, active preventive interventions such as weight loss and exercise should be taken. This study, within its limitations, may be useful for evaluating apolipoprotein A-I and B concentrations in Korean adults.

Apolipoprotein A1 Inhibits TGF-β1-Induced Epithelial-to-Mesenchymal Transition of Alveolar Epithelial Cells

  • Baek, Ae Rin;Lee, Ji Min;Seo, Hyun Jung;Park, Jong Sook;Lee, June Hyuk;Park, Sung Woo;Jang, An Soo;Kim, Do Jin;Koh, Eun Suk;Uh, Soo Taek;Kim, Yong Hoon;Park, Choon Sik
    • Tuberculosis and Respiratory Diseases
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    • 제79권3호
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    • pp.143-152
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    • 2016
  • Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor ${\beta}1$ (TGF-${\beta}1$)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-${\beta}1$-induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-${\beta}1$ with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and ${\alpha}$-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-${\beta}1$ receptor type 1 ($T{\beta}RI$) and type 2 ($T{\beta}RII$) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-${\beta}1$-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-${\beta}1$-induced change of the EMT phenotype. ApoA1 inhibited the TGF-${\beta}1$-induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-${\beta}1$-induced increase in $T{\beta}RI$ and $T{\beta}RII$ expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-${\beta}1$-induced EMT in experimental lung fibrosis.

Participation of SRE4, an URE1 Enhancer Core Sequence, in the Sterol-Mediated Transcriptional Upregulation of the Human Apolipoprotein E Gene

  • Min, Jung-Hwa;Paik, Young-Ki
    • BMB Reports
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    • 제31권6호
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    • pp.565-571
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    • 1998
  • The expression of the endogenous human apolipoprotein(apo)E gene was significantly induced when HepG2 cells were treated with exogenous 25-hydroxy-cholesterol. This sterol-mediated apoE gene upregulation appears to require the participation of a positive element for the apoE gene transcription (PET) ( -169/ -140), a core sequence of upstream regulatory element (URE)1 enhancer of the human apoE gene. This PET was renamed as sterol regulatory element (SRE)4 based on its new role as a sensor for the level of intracellular sterol. Furthermore, a gel mobility shift analysis showed that binding activity of the SRE4 binding protein (BP) obtained from HepG2 cells was induced by sterol treatment, while that from either MCF7 or BT20 cells remained unchanged. Binding activity of SRE4BP was also induced in mouse macrophage cells, J774A.1, by sterol treatment, but it was drastically reduced when cells were subjected to treatment of AY-9944, a potent inhibitor for sterol synthesis. However, binding activity of Spl, which is a co-binding protein to the SRE4 region, remained the same in either condition, suggesting that SRE4BP (formally known as PETBP) may be mainly responsible for the sterol-mediated regulation of the apoE gene expression. Deletion analysis of the core binding site of SRE4BP by gel mobility shift assays showed that the minimal sequence of the SRE4BP binding appears to reside between -157 and -140, confirming the identity of SRE4 with the previously determined core sequence of URE1.

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Apo E Null mice에서 인삼 Ginsenosides (PD:PT = 1) 추출물의 지질개선 및 항산화 효과 (Hypolipidemic and Antioxidant Effects to Ginseng Extract (PD:PT = 1) in Apo E Null Mice)

  • 장수정;김성수;이명숙
    • Journal of Nutrition and Health
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    • 제41권7호
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    • pp.594-601
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    • 2008
  • Panax ginseng C.A. Meyer (Panax ginseng) has been used for several thousand years to prolong longevity in Asian countries. Ginsenosides are the most active components isolated from ginseng and belong to damarane saponin which are separated into protopanaxadiol and protopanaxtriol. To evaluate the complex effect of ginsenoside in apo E null mice, ginseng extract were intraperioneally (i.p.) injected and provided high-cholesterol diet for 12 weeks. Ginseng extract came from were i.p. injected with dose of 100 mg/kg/day for 4 weeks in the last experimental duration. Ginseng extract used experiment was abundant Rb1, Rc, Re, and Rg1 and PD:PT ratio was 1.2. The high-cholesterol diet induced liver damage was significantly reduced by ginseng extract. Results from plasma lipid profiles and atherogenic index were improved by ginseng extracts. The GE group significantly decreased plasma TG and TC by 73% and 61% compared to apo E (-/-) group. Also ginseng extract tend to decrease lipid profiles and lipidperoxidation contents in liver and heart. Ginseng extract with an abundant amount of Rg1 significantly suppressed the apoptosis induction of cardiac tissue. In conclusion, ginseng extract (PD:PT = 1) was improved lipid profiles and anti-oxidant effects.

Thermal Denaturation of the Apo-cyclic AMP Receptor Protein and Noncovalent Interactions between Its Domains

  • Won, Hyung-Sik;Seo, Min-Duk;Ko, Hyun-Suk;Choi, Wahn Soo;Lee, Bong-Jin
    • Molecules and Cells
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    • 제26권1호
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    • pp.61-66
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    • 2008
  • Cyclic AMP receptor protein (CRP) is allosterically activated by cAMP and functions as a global transcription regulator in enteric bacteria. Structural information on CRP in the absence of cAMP (apo-CRP) is essential to fully understand its allosteric behavior. In this study we demonstrated interdomain interactions in apo-CRP, using a comparative thermodynamic approach to the intact protein and its isolated domains, which were prepared either by limited proteolysis or using recombinant DNA. Thermal denaturation of the intact apo-CRP, monitored by differential scanning calorimetry, revealed an apparently single cooperative transition with a slight asymmetry. Combined with circular dichroism and fluorescence analysis, the thermal denaturation of apo-CRP could be interpreted as a coupled process involving two individual transitions, each attributable to a structural domain. When isolated individually, both of the domains exhibited significantly altered thermal behavior, thus pointing to the existence of non-covalent interdomain interactions in the intact apo-CRP. These observations suggest that the allosteric conformational change of CRP upon binding to cAMP is achieved by perturbing or modifying pre-existing interdomain interactions. They also underline the effectiveness of a comparative approach using calorimetric and structural probes for studying the thermodynamics of a protein.

Apolipoprotein E 다형성과 고지혈증 위험 유무에 따른 혈중 지질농도, 영양소 섭취, 생활습관 및 위험요인과의 관계 (Apolipoprotein E Phenotypes and the Relationship Among Lipid Levels, Nutrient Intakes, Lifestyles and Risk Factors Between Subjects with and without Hyperlipidemic Risk)

  • 이재은;조상운;강지연;백윤미;최창순;박유경;최태인
    • Journal of Nutrition and Health
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    • 제41권5호
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    • pp.402-413
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    • 2008
  • This study was performed to investigate Apolipoprotein E phenotypes and the relationship among lipid levels, nutrient intakes, lifestyles and risk factors between subjects with and without hyperlipidemic risk. The data were collected from 675 industrial male workers who had completed annual medical examination. Compared to the normal group, the hyperlipidemic risk group in Apo E3 and E4 had significantly higher BMI (p < 0.05) and showed significantly higher body fat (%), waist circumference and WHR in all types of Apo E (p < 0.05). In addition, the hyperlipidemic risk group had significantly higher total cholesterol, LDL-cholesterol, triglyceride and AI than the normal group in all types of Apo E (p < 0.05). Intakes of protein, calcium, phosphorus, iron, vitamin A, vitamin B1, vitamin B2, vitamin C and niacin in Apo E3 were significantly lower in the hyperlipidemic risk group than in the normal group (p < 0.05). In the logistic regression analysis, after adjustment for other factors, Apo E2 + E4, waist and WHR were the significant risk factors associated with hyperlipidemia, but protein intakes were associated with significantly lower risks of hyperlipidemia (p < 0.05). In conclusion, genetic factor (Apo E2 or Apo E4), anthropometric index and nutrient intake seem to influence hyperlidemic risk. Further studies and efforts will be needed to evaluate the independent relationships among hyperlipidemic risk factors.