• 제목/요약/키워드: CCAAT/Enhancer Binding Protein ${\beta}$ ($C/EBP{\beta}$)

검색결과 41건 처리시간 0.028초

Role of CCAAT/ Enhancer Binding Protein ${\beta}$ Activation in the Induction of Glutathione S-Transferase A2 by Toluene

  • Choi, Dal-Woong;Sohn, Jong-Ryeul;Moon, Kyung-Whan;Byeon, Sang-Hoon;Kim, Hi-Chol;Kim, Young-Whan
    • 한국환경보건학회:학술대회논문집
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    • 한국환경보건학회 2005년도 국제학술대회
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    • pp.341-344
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    • 2005
  • The expression of the glutathione S-transferase (GST), whose induction accounts for antioxidant defense system, is regulated by activation of CCAAT/enhancer binding protein ${\beta}$ ($C/EBP{\beta}$), Sick house syndrome (SHS) presents healthy damage owing to the indoor environment of a building. Toluene has been implicated in one of the important causes of SHS. The present study investigated the effects of toluene treatment on the induction of GSTA2 gene and its mechanism. H411E cells treated with toluene, and GSTA2 expression was determined by immunoblot analysis. The translocation of $C/EBP{\beta}$ was assessed by immunocytochemical assays. $C/EBP{\beta}$ DNA binding activity was determined by electrophoretic mobility shift assays. The role of the C/EBP binding site in the induction of the GSTA2 gene was assessed by luciferase reporter-gene activity. Toluene induced GSTA2 protein expression. In toluene-treated cells, $C/EBP{\beta}$ translocated to the nucleus and bound to the consensus sequence of C/EBP (TTGCGCAA). Toluene treatment increased luciferase reporter-gene activity in cells transfected with the C/EBP-containing regulatory region of the GSTA2 gene. Oxidative stress is believed to play an important role in the induction of GSTA2 gene by toluene This study shows that toluene-induced GSTA2 gene expression is dependent upon nuclear translocation and binding of $C/EBP{\beta}$ to the C/EBP response element in the GSTA2 gene promoter.

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CCAAT/enhancer-binding protein beta (C/EBPβ) is an important mediator of 1,25 dihydroxyvitamin D3 (1,25D3)-induced receptor activator of nuclear factor kappa-B ligand (RANKL) expression in osteoblasts

  • Jo, Sungsin;Lee, Yun Young;Han, Jinil;Lee, Young Lim;Yoon, Subin;Lee, Jaehyun;Oh, Younseo;Han, Joong-Soo;Sung, Il-Hoon;Park, Ye-Soo;Kim, Tae-Hwan
    • BMB Reports
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    • 제52권6호
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    • pp.391-396
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    • 2019
  • Receptor activator of nuclear factor kappa B ligand (RANKL) expression in osteoblasts is regulated by 1,25-dihydroxyvitamin D3 (1,25D3). CCAAT/enhancer-binding protein beta ($C/EBP{\beta}$) has been proposed to function as a transcription factor and upregulate RANKL expression, but it is still uncertain how $C/EBP{\beta}$ is involved in 1,25D3-induced RANKL expression of osteoblasts. 1,25D3 stimulation increased the expression of RANKL and $C/EBP{\beta}$ genes in osteoblasts and enhanced phosphorylation and stability of these proteins. Moreover, induction of RANKL expression by 1,25D3 in osteoblasts was downregulated upon knockdown of $C/EBP{\beta}$. In contrast, $C/EBP{\beta}$ overexpression directly upregulated RANKL promoter activity and exhibited a synergistic effect on 1,25D3-induced RANKL expression. In particular, 1,25D3 treatment of osteoblasts increased $C/EBP{\beta}$ protein binding to the RANKL promoter. In conclusion, $C/EBP{\beta}$ is required for induction of RANKL by 1,25D3.

Silibnin의 지방세포분화 억제 및 세포사멸 유도 효과 (Silibinin Inhibits Adipogenesis and Induces Apoptosis in 3T3-L1 Adipocytes)

  • 이슬기;권택규;남주옥
    • 한국미생물·생명공학회지
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    • 제45권1호
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    • pp.27-34
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    • 2017
  • CCAAT/enhancer-binding protein beta, delta ($C/EBP{\beta}$, ${\delta}$)는 지방세포분화 과정의 초기에 필수적으로 요구되며 지방생성 주요 조절인자인 proliferator-activated receptor gamma ($PPAR{\gamma}$) and CCAAT/enhancer-binding protein-alpha ($C/EBP{\alpha}$)의 발현을 유도한다. 본 연구에서는 silibinin의 지방세포 분화 억제 효과 및 이러한 효과가 지방세포 분화초기에 $C/EBP{\beta}$$C/EBP{\delta}$의 발현 조절을 통해 일어난 다는 것을 확인하였다. Silibinin은 지방세포 내 지질축적을 억제하고 세포분화 과정 동안 관여하는 다양한 유전자의 mRNA 발현을 억제하였다. 또한 lipoprotein lipase (LPL), fatty acid binding protein 4 (AP2) 및 adiponectin과 같은 지방세포 분화 관련 유전자의 발현을 억제시켰다. 따라서, Silibinin의 지방세포 분화 억제효과는 $C/EBP{\beta}$$C/EBP{\delta}$의 발현억제에 의한 것으로 보인다. 더불어, Silibinin은 capspase-3 활성을 통해 분화하는 세포에 특이적으로 세포사멸을 유도하는 것을 확인하였다.

Expressional Evaluation of C/EBP Family, SREBP1, and Steroid Hormone Receptors in the Epididiymal Fat of Postnatally Developing Mouse

  • Lee, Yong-Seung;Lee, Ki-Ho
    • 한국발생생물학회지:발생과생식
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    • 제26권2호
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    • pp.49-58
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    • 2022
  • The differentiation and development of preadipocyte into mature adipocyte are regulated by transcription factors, such as CCAAT enhancer binding protein (Cebp) gene family and sterol regulatory element binding transcription factor 1 (Srebp1). Steroid hormones give influences on the development and function of adipocyte. The present research examined expression patterns of CCAAT enhancer binding protein alpha (Cebpa), CCAAT enhancer binding protein beta (Cebpb), CCAAT enhancer binding protein gamma (Cebpg), sterol regulatory element binding transcription factor 1 (Srebp1), androgen receptor (Ar), and estrogen receptors (Esr) among different epididymal fat parts during postnatal period by quantitative real-time polymerase chain reaction. In the distal epididymal fat, expression of Cebpa, Cebpb, Cebpg, Srebp1, Ar, and Esr2 was increased until 12 months of age, while expression of Esr1 was decreased at 5 months of age and was not detectable after 8 months of age. In the proximal epididymal fat, transcript levels of Cebps and Srebp1 were increased at 8 months of age, followed by decreases of Cebpb and Cebpg transcript levels at 12 months of age. An additional increase of Srebp1 expression was observed at 12 months of age. Expression of Ar and Esr2 were increased until 8 months of age, followed by a drop of Ar expression level at 12 months of age. Expression pattern of Esr1 was similar to that in the distal epididymal fat. In the tail epididymal fat, expression of Cebpa, Cebpg, Srebp1, Ar, and Esr2 was increased with age. Esr1 was not detectable at all. The highest level of Cebpb was observed at 8 months of age. These data suggest the possibility of developmental and functional differentiation among the epididymal fat parts.

항비만소재의 lipoprotein lipase 억제 작용 연구 (Study of Lipoprotein Lipase Inhibitory Activity of Anti-obesity Herb Extracts)

  • 이성미;강윤환;김경곤;김태우;최면
    • 한국식품과학회지
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    • 제47권2호
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    • pp.246-253
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    • 2015
  • 본 연구에는 항비만소재로 연구되어진 11종의 소재를 대상으로 lipoprotein lipase (LPL)의 억제효능을 확인하고자 배양배지내 LPL의 함량과 LPL 효소활성을 측정하였다. 그 결과 3T3-L1 adipocyte에서 LPL의 분비를 억제하는 소재로 능이추출물(NE)을 선택할 수 있었다. 선택된 NE의 폴리페놀과 플라보노이드 함량을 측정한 결과 $16.61{\pm}0.44mg/g$$6.58{\pm}0.01mg/g$이 각각 확인되었다. NE의 LPL 분비억제기작을 확인하기위해 먼저 세포내 LPL단백질의 함량과 mRNA 발현을 확인하였다. 그 결과 함량이 감소했던 배양배지와는 다르게 NE를 처리한 3T3-L1 adipocyte의 세포내 LPL은 유의하게 증가한 것을 확인할 수 있었으며 mRNA의 발현에는 영향이 없음을 관찰할 수 있었다. 이를 바탕으로 생성된 LPL 단백질의 exocytosis에 문제가 발생했을 것으로 유추하고 다양한 단백질 이동 관련 유전자의 발현을 확인하였다. 그 결과 LPL의 이동과 분해에 관여하여 세포내 LPL의 활성을 조절하는 것으로 알려진 SorLA의 발현이 증가하는 것을 확인하고 이를 조절하는 transcription factor의 발현과 nuclear로의 이동에 NE가 미치는 영향을 검토하였다. 그 결과 NE를 처리함으로써 SorLA promoter에 작용하는 $C/EBP{\beta}$의 단백질 발현이 nuclear에서 증가하는 것을 확인할 수 있었다. 본 연구를 통해 NE가 SorLA 유전자의 transcription factor인 $C/EBP{\beta}$의 단백질 발현을 nuclear에서 증가시킴으로서 결과적으로 LPL의 분비억제가 가능함을 확인할 수 있었으며 이는 NE의 항비만 효과기전을 설명하는 기초자료를 제공하는 것이라 사료된다.

$17{\beta}$-estradiol Prevents the Expression of $CEBP{\alpha}$-mediated Adipocyte Marker Genes in Female Ovariectomized C57BL/6 Mice

  • Yoon, Mi-Chung;Jeong, Sun-Hyo
    • 대한의생명과학회지
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    • 제14권3호
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    • pp.131-137
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    • 2008
  • Adipogenesis is a complex sequence of events that culminates in the differentiation of fibroblast-like preadipocytes into specialized lipid-filled adipocytes and also involves a cascade of expression of many transcription factors such as peroxisome proliferator-activated receptor ${\gamma}(PPAR{\gamma})$ and CCAAT/enhancer-binding proteins (C/EBPs). $PPAR{\gamma}$ and C/EBPs transcriptionally transactivate adipocyte specific genes, including fatty acid transport protein (FAT/CD36) and leptin. To determine whether $17{\beta}$-estradiol modulates $C/EBP{\alpha}$ actions on adipogenesis in high fat diet-fed female ovariectomized (OVX) C57BL/6 mice, mice were treated with $17{\beta}$-estradiol for 7 days and the effects of $17{\beta}$-estradiol on adipose tissue mass and expression of adipocyte specific gene as well as $C/EBP{\alpha}$ were measured. Compared to vehicle-treated OVX control mice, OVX mice treated with $17{\beta}$-estradiol for 7 days had lower adipose tissue weights that were similar to weights in high fat diet-fed sham-operated (Sham) mice. OVX mice showed the increased expression of $C/EBP{\alpha}$ mRNA compared with Sham mice. However, $17{\beta}$-estradiol treatment in OVX mice inhibited OVX induced-$C/EBP{\alpha}$ activation, indicating that $17{\beta}$-estradiol may act as an inhibitor of $C/EBP{\alpha}$ action. Moreover, $17{\beta}$-estradiol decreased mRNA levels of adipocyte marker genes, such as lipoprotein lipase, FAT/CD36 and leptin, to levels in Sham mice. These results suggest that down-regulation of adipogenesis by $17{\beta}$-estradiol may be due to reduced adipose $C/EBP{\alpha}$ activities in female OVX C57BL/6 mice.

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C/EBP$\beta$ mediated inhibition of PAH-inducible CYPlAl expression by Oltipraz, a cancer chemopreventive agent

  • Cho, Il-Je;Kim, Sang-Geon
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.85.3-86
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    • 2003
  • Oltipraz, a cancer chemopreventive agent, induces CYP1A1 to a certain extent by transactivation of the gene via the Ah receptor (AhR)-xenobiotic response element (XRE) pathway. Previously, we showed that oltipraz promoted CCAAT/enhancer binding protein (C/EBP ) activation, which leads to the induction of glutathione S-transferase. Given that oltipraz activates C/EBP for gene transactivation and that the putative C/CBP binding site is located in CY)1A1 promoter region, this study investigated the effect of oltipraz on CYP1A1 induction by 3-methylcholanthrene (3-MC). (omitted)

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죽력의 3T3-L1 지방전구세포에서 지방축적 억제 효과 (Suppression of Lipid Accumulation in Differentiating 3T3-L1 Preadipocytes by a Standardized Commercial Juknyeok)

  • 장병철
    • 한방비만학회지
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    • 제22권1호
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    • pp.38-46
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    • 2022
  • Objectives: Juknyeok (JN) is natural liquor extracted from bamboo stems (Phyllostachys bambusoides) and has been used as a traditional Korean medicine for improving vascular function, blood glucose, and treating stroke. Until now, the JN's lipid-lowering effect and underlying mechanism in adipocytes are poorly understood. The aim of this study was to scrutinize the effect of a standardized commercial JN on lipid accumulation during the differentiation of 3T3-L1 preadipocytes. Methods: Lipid and triglyceride (TG) accumulation in differentiating 3T3-L1 preadipocytes were measured by Oil Red O staining and AdipoRed assay, respectively. Cell count analysis was used to ascertain 3T3-L1 cytotoxicity. Immunoblotting and Reverse transcription polymerase chain reaction analysis were used to assess protein and messenger RNA (mRNA) expression levels in 3T3-L1 cells, respectively. Results: Treatment with JN at 25 𝜇l/ml after pH calibration with 6.35 significantly reduced lipid and TG accumulation in differentiating 3T3-L1 preadipocytes without significant cytotoxicity. On mechanistic levels, JN markedly suppressed protein expression levels of CCAAT/enhancer-binding protein (C/EBP)-𝛽 and fatty acid synthase (FAS) during the differentiation of 3T3-L1 preadipocytes. However, JN did not affect the protein expression levels of C/EBP-𝛼, peroxisome proliferator-activated receptor-𝛽/𝛾, and phosphorylation levels of signal transducer and activator of transcription-3/5 in differentiating 3T3-L1 preadipocytes. JN also reduced leptin mRNA expression levels in differentiating 3T3-L1 preadipocytes. Conclusions: JN at 25 𝜇l/ml lowers lipid accumulation and TG content in differentiating 3T3-L1 cells, mediated through the reduced expression levels of C/EBP-𝛽 and FAS.