Search results for: ADD1 (SREBP1c)
#31488172 
2019/09/05
To Up
Anti-obesity effect of Yangkyuksanwha-tang in high-fat diet-induced obese mice.
Yangkyuksanwha-tang (YST) is an herbal medicine based on Sasang constitutional medicine (SCM) and is widely used in Korean traditional medicine. The aim of the study was to evaluate the effect of YST on obesity in high-fat diet (HFD)-induced obese mice.Young-Mee Koh, Soon-Woo Jang, Taek-Won Ahn
2821 related Products with: Anti-obesity effect of Yangkyuksanwha-tang in high-fat diet-induced obese mice.
50 ul100ug100 ul100 ul50 ul100ug100 μg100 μg100ug Lyophilized100 μg100ug Lyophilized
Related Pathways
#30621146 2019/01/04
To Up
Salt Induces Adipogenesis/Lipogenesis and Inflammatory Adipocytokines Secretion in Adipocytes.
It is well known that high salt intake is associated with cardiovascular diseases including hypertension. However, the research on the mechanism of obesity due to high salt intake is rare. To evaluate the roles of salt on obesity prevalence, the gene expression of adipogenesis/lipogenesis and adipocytokines secretion according to adipocyte dysfunction were investigated in salt-loading adipocytes. High salt dose-dependently increased the expression of adipogenic/lipogenic genes, such as , and , but decreased the gene of lipolysis like , ultimately resulting in fat accumulation. With SIK-2 and Na⁺/K⁺-ATPase activation, salt increased the metabolites involved in the renin-angiotensin-aldosterone system (RAAS) such as and Increasing insulin dependent insulin receptor substrate (IRS)-signaling, resulting in the insulin resistance, mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and Akt-mTOR were activated but AMPK(Thr) was depressed in salt-loading adipocytes. The expression of pro-inflammatory adipocytokines, TNFα, MCP-1, COX-2, IL-17A, IL-6, leptin, and leptin to adiponectin ratio (LAR) were dose-dependently increased by salt treatment. Using the inhibitors of MAPK/ERK, U0126, we found that the crosstalk among the signaling pathways of MAPK/ERK, Akt-mTOR, and the inflammatory adipogenesis can be the possible mechanism of salt-linked obesity. The possibilities of whether the defense mechanisms against high dose of intracellular salts provoke signaling for adipocytes differentiation or interact with surrounding tissues through other pathways will be explored in future research.Myoungsook Lee, Sungbin Richard Sorn, Yunkyoung Lee, Inhae Kang
1761 related Products with: Salt Induces Adipogenesis/Lipogenesis and Inflammatory Adipocytokines Secretion in Adipocytes.
1 mg2ug2.5 mg1 g5ug2ug100 mg0.1 mg5ug5ug 5 G 10 MG
Related Pathways
#22687396 //
To Up
1β-Hydroxy-2-oxopomolic acid isolated from Agrimonia pilosa extract inhibits adipogenesis in 3T3-L1 cells.
In order to determine anti-adipogenic effect, this study investigated 1β-hydroxy-2-oxopomolic acid (HOA) isolated from Agrimonia pilosa inhibits adipocyte differentiation and expression of adipogenic marker genes, such as peroxisome proliferator activated receptor γ (PPARγ), CCAAT-enhancer-binding protein α (C/EBPα), glucose transporter 4 (GLUT4), adiponectin, adipocyte fatty acid-binding protein 2 (aP2), adipocyte determination and differentiation factor 1/sterol regulatory element binding protein 1c (ADD1/SREBP1c), resistin, and fatty acid synthase (Fas) in 3T3-L1 preadipocyte. We demonstrated that HOA induced a significant decrease in lipid accumulation and expression of adipogenic marker genes in a dose-dependent manner. In addition, HOA reduced the transcripitional activity of PPARγ induced by troglitazone, a potent diabetes agent; it also suppressed expression of PPARγ and C/EBPα protein levels. Our data suggest that HOA isolated from Agrimonia pilosa inhibits adipocyte differentiation through downregulation of various adipocytokines by blocking PPARγ and C/EBPα expression.Eun-Kyung Ahn, Jung A Lee, Dong-Wan Seo, Seong Su Hong, Joa Sub Oh
2589 related Products with: 1β-Hydroxy-2-oxopomolic acid isolated from Agrimonia pilosa extract inhibits adipogenesis in 3T3-L1 cells.
1.00 flask50 mg 1 G96tests1 mg100 ul250 mg1 g400 ug25 mg100ug Lyophilized
Related Pathways
#20872252 2010/09/26
To Up
A large indel mutation of the bovine ADD1/SREBP1c gene and its effects on growth traits in some native cattle breeds from China.
Adipocyte determination and differentiation-dependent factor 1/sterol regulatory element-binding protein-1c (ADD1/SREBP1c) is a major determinant of tissue differential lipogenic capacity in mammalian and avian species. The objectives of the present study were to focus on insertion-deletion polymorphism (indel) in the bovine ADD1/SREBP1c gene, and analyzing its effect on growth traits in a sample of 1035 cattle belonging to four Chinese cattle breeds. PCR-SSCP, DNA sequencing and agarose electrophoresis methods were used. The 778 bp PCR products of ADD1/SREBP1c gene exhibited three genotypes and two alleles were revealed: W and D. Frequencies of the W allele varied from 0.8651 to 1.000. The associations of the 84 bp indel mutation of ADD1/SREBP1c gene with growth traits of 265 Nanyang cows were analyzed. The animals with genotype WD had significantly higher birth weight, body weight, average daily gain than those with genotype WW at birth, 6-, 12-, 18-, and 24-month old (P < 0.05 or P < 0.01). These results suggest that the indel mutation of bovine ADD1/SREBP1c gene may influence the growth traits in cattle.Yong-Zhen Huang, En-Ping Zhang, Jing Wang, Yong-Tao Huai, Liang Ma, Fu-Ying Chen, Xian-Yong Lan, Chu-Zhao Lei, Xing-Tang Fang, Ju-Qiang Wang, Hong Chen
2972 related Products with: A large indel mutation of the bovine ADD1/SREBP1c gene and its effects on growth traits in some native cattle breeds from China.
1000 Units5100ug1000 Units1 mL250 mg1 mg100.00 ug1mg
Related Pathways
#19962449 2009/12/02
To Up
ADD1/SREBP1c activates the PGC1-alpha promoter in brown adipocytes.
Cold adaptation elicits a paradoxical simultaneous induction of fatty acid synthesis and beta-oxidation in brown adipose tissue. We show here that cold exposure coordinately induced liver X receptor alpha (LXRalpha), adipocyte determination and differentiation-dependent factor 1 (ADD1)/sterol regulatory element-binding protein-1c (SREBP1c) and peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC1alpha) in brown and inguinal white adipose tissues, but not in epididymal white adipose tissue. Using in vitro models of white and brown adipocytes we demonstrate that beta-adrenergic stimulation induced expression of LXRalpha, ADD1/SREBP1c and PGC1alpha in cells with a brown-like adipose phenotype. We demonstrate that ADD1/SREBP1c is a powerful inducer of PGC1alpha expression via a conserved E box in the proximal promoter and that beta-adrenergic stimulation led to recruitment of ADD1/SREBP1c to this E box. The ability of ADD1/SREBP1c to activate the PGC1alpha promoter exhibited a striking cell type dependency, suggesting that additional cell type-restricted factors contribute to ADD1/SREBP1c-mediated activation. In conclusion, our data demonstrate a novel role of ADD1/SREBP1c as a regulator of PGC1alpha expression in brown adipose tissue.Qin Hao, Jacob B Hansen, Rasmus K Petersen, Philip Hallenborg, Claus Jørgensen, Saverio Cinti, Philip J Larsen, Knut R Steffensen, Haibo Wang, Sheila Collins, Jun Wang, Jan-Ake Gustafsson, Lise Madsen, Karsten Kristiansen
1051 related Products with: ADD1/SREBP1c activates the PGC1-alpha promoter in brown adipocytes.
100.00 ug100ug Lyophilized100ug5mg100ug100ug Lyophilized10 100ug10 100 μg20
Related Pathways
#19932681 2009/11/22
To Up
cAMP-response element binding protein (CREB) positively regulates mouse adiponectin gene expression in 3T3-L1 adipocytes.
Adiponectin is expressed in adipose tissue by adipogenic transcription factors including PPARgamma, C/EBPalpha, and ADD1/SREBP1c. Because cAMP-response element binding protein (CREB) is also a central transcriptional activator of adipocyte differentiation, we evaluated CREB to determine if it stimulates adiponectin gene expression. To accomplish this, we evaluated the effects of activated CREB on the promoter activity of the mouse adiponectin gene, and identified the cAMP-response element (CRE) in the promoter. The constitutively active form of CREB increased the promoter activity of the mouse adiponectin gene. In addition, transfection studies using 5' serial deleted promoters revealed the presence of a putative CRE located between the -1250 and -1000bp region. Furthermore, an electrophoresis mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) analysis demonstrated that CREB bound to the region between -1022 and -995 in the adiponectin promoter. Insulin-like growth factor (IGF-1), which activate CREB, increased the adiponectin promoter activity. However, this stimulation was prevented by the dominant negative form of CREB (ACREB) and pretreatment with PD098059, indicating that IGF-1 stimulate adiponectin expression through CREB phosphorylation via the ERK pathway. Importantly, the transactivation of adiponectin expression by CREB was inhibited by ATF3. Coimmunoprecipitation and GST pull-down assay revealed that ATF3 bound to CREB and prevented CREB phosphorylation induced during differentiation of 3T3-L1 adipocytes. Collectively, these findings demonstrate that CREB is a positive regulator of mouse adiponectin gene expression in adipocytes, which play an important role in the regulation of adiponectin expression in response to growth factor.Hyun Bae Kim, Won Ho Kim, Kyu Lee Han, Jae Hong Park, Jiyoun Lee, Jiyoung Yeo, Myeong Ho Jung
2122 related Products with: cAMP-response element binding protein (CREB) positively regulates mouse adiponectin gene expression in 3T3-L1 adipocytes.
100.00 ug100.00 ug100.00 ug100.00 ug100.00 ug100 100 ul100 ul0.2 mg200 5ug100ug Lyophilized
Related Pathways
#19407971 2009/04/29
To Up
Regulation of adipocyte differentiation by histone deacetylase inhibitors.
In this study, we investigated the effects of various histone deacetylase (HDAC) inhibitors on adipocyte differentiation. Treatment of 3T3-L1 cells with HDAC inhibitors such as apicidin, trichostatin A, or suberoylanilide hydroxamic acid, under conditions that normally promote differentiation led to a dramatic attenuation of adipocyte differentiation. In contrast, sodium butyrate (NaB) treatment increased adipocyte differentiation. Accordingly, the expression of adipogenic marker genes such as FAS, aP2, PPARgamma, resistin, C/EBPalpha, ADD1/SREBP1c, and adiponectin were inhibited by apicidin treatment but not NaB, indicating that the adipocyte differentiation process could be differentially regulated depending on the type of HDAC inhibitor utilized. In addition, this differential effect seemed not to be due to disruption of the insulin- signaling pathway. Interestingly, our data showed that apicidin treatment could induce dedifferentiation of fully differentiated adipocytes, as evident by the fact that apicidin treatment led to a decrease of Oil Red O-stained adipocytes with a concomitant reduction in the expression levels of adipogenic marker genes. Collectively, our results suggest that adipocyte differentiation and dedifferentiation may be regulated by HDAC inhibitors.Su-Nam Kim, Hye-Young Choi, Yong Kee Kim
2394 related Products with: Regulation of adipocyte differentiation by histone deacetylase inhibitors.
50 ug5 x 50 ug0.1ml (1mg/ml)10mg100 ul100.00 ul100 µg50 ug
Related Pathways
#17074803 2006/10/30
To Up
Chromatin remodeling complex interacts with ADD1/SREBP1c to mediate insulin-dependent regulation of gene expression.
Insulin plays a critical role in whole-body energy homeostasis by regulating lipid and glucose metabolism. In fat and liver tissues, ADD1/SREBP1c is a key transcription factor to mediate insulin-dependent regulation of gene expression. Although transcriptional and proteolytic activation of ADD1/SREBP1c has been studied intensively, the mechanism by which insulin regulates expression of its target genes with ADD1/SREBP1c at the chromatin level is unclear. Here, we reveal that SWI/SNF chromatin remodeling factors interact with the ADD1/SREBP1c and actively regulate insulin-dependent gene expression. Insulin enhanced recruitment of SWI/SNF chromatin remodeling factors to its target gene promoters with concomitant changes in the chromatin structures as well as gene expression. Furthermore, in vivo overexpression of BAF155/SRG3, a component of the SWI/SNF complex, substantially promoted insulin target gene expression and insulin sensitivity. Taken together, our results suggest that the SWI/SNF chromatin remodeling complexes confer not only insulin-dependent gene expression but also insulin sensitivity in vivo via interaction with ADD1/SREBP1c.Yun Sok Lee, Dong Hyun Sohn, Daehee Han, Han-Woong Lee, Rho Hyun Seong, Jae Bum Kim
1353 related Products with: Chromatin remodeling complex interacts with ADD1/SREBP1c to mediate insulin-dependent regulation of gene expression.
300 units100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized
Related Pathways
#16949052 2006/08/24
To Up
Selective LXRalpha inhibitory effects observed in plant extracts of MEH184 (Parthenocissua tricuspidata) and MEH185 (Euscaphis japonica).
Liver X receptors (LXRs) are nuclear hormone receptors that behave as lipid sensors of cellular cholesterol and fatty acid. Although LXR activation can alleviate hypercholesterolemia by inducing cholesterol efflux, it also results in undesirable effects of fatty acid synthesis, resulting in hepatic steatosis and hyperlipidemia. Therefore, it is critical to identify LXRalpha inhibitory agents that would repress fatty acid synthesis and hepatic lipid accumulation. In current study, screening of plant extracts used for traditional oriental medicine resulted in the identification of two candidates demonstrating selective LXRalpha inhibitory activity. These were whole leaf methanol extracts of Parthenocissua tricuspidata (MEH184) and Euscaphis japonica (MEH185). Both MEH184 and MEH185 decreased transcriptional activity of LXRalpha and the expression of LXRalpha target genes, such as FAS and ADD1/SREBP1c. Additionally, MEH184 and MEH184 significantly reduced lipogenesis and adipocyte differentiation. Together, the data imply that MEH184 and MEH185 possess selective antagonistic properties on LXRalpha to downregulate lipogenesis.Kang Ho Kim, Seung Hyun Choi, Thomas S Lee, Won Keun Oh, Dong Sun Kim, Jae Bum Kim