Publication for Fasn and Scd1

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
mmu Fasn fatty acid synthase 14104 [link]
mmu Scd1 stearoyl-Coenzyme A desaturase 1 20249

Pubmed ID Priority Text
23637738 0.99 Scd1and Fasn at E17.5 indicating that these factors may be upregulated by Creb1 in the developing lung late in gestation.
0.98 stearoyl-CoA desaturase 1 (Scd1) and fatty acid synthase (Fasn) showed highly reduced gene expression in Creb1-/- lungs.
0.98 Scd1 and Fasn mRNA levels were down regulated in the E17.5 Creb1-/- mouse lung while the lipogenic-associated transcription factors SrebpF1, C/ebpalpha and Ppargamma were increased.
0.98 Scd1, but not Fasn gene expression and protein levels in lung epithelial cells.
0.98 Scd1 and Fasn has been studied extensively in the context of obesity and cancer development in tissues with known roles in lipogenesis such as liver and adipose tissue.
0.98 Fasn and Scd1.
0.98 Fasn and Scd1 using both in vivo and in vitro models where Creb1 function is either lost or inhibited, and show that in the case of Scd1, Creb1 is essential for normal expression in the lung.
0.98 Scd1 (7.8 fold, p<0.05) and Fasn (1.9 fold, p<0.05) to be significantly down-regulated in Creb1-/- fetal mice (Table 1), that was subsequently verified by qPCR (Figure 1A).
0.98 Scd1 and Fasn gene expression.
0.97 Scd1 and Fasn mRNA levels in the lung of E17.5 Creb1 Epi Delta/Delta fetal mice relative to controls (Figure 5A).
0.96 fatty acid synthase (Fasn) and steroyl-CoA desaturase 1 (Scd1), both of which previously showed highly reduced mRNA levels in Creb1-/- fetal lungs.
0.96 Scd1 and Fasn gene expression in the fetal mouse lung
0.95 Scd1 (Figure 2A-F) protein levels in the Creb1-/- fetal mouse lung compared to wildtype controls, however we did not observe any alteration in levels of Fasn protein (Figure 3A-F).
0.93 Scd1 and Fasn mRNA levels in the lung of E17.5 Creb1-/- fetal mice compared to littermate controls (A).
0.92 Fasn and Scd1 during late respiratory development, as well as the protein localisation of these factors to epithelial cell subsets within the fetal lung.
0.83 Scd1 and Fasn mRNA levels in the lung epithelial-cell-specific Creb1 Epi Delta/Delta fetal mice (A).
0.78 Scd1 and Fasn, and lipogenic transcription factor genes during mouse lung development.
24489111 0.99 FAS and SCD1 (Fig. 2A).
0.98 FAS and SCD1, and suppress de novo lipogenesis in mice.
0.98 FAS and SCD1 (Fig. 3D) in both wild-type and Elovl2-/- mice, suggesting an SREBP-1c-independent mechanism in the control of lipogenesis under these conditions.
0.98 SCD1 and FAS enzymes can be regulated in an SREBP-1c-independent manner under certain dietary conditions.
0.97 FAS and SCD1 enzymes, as C16, C16:1, and C18:1 fatty acids are less abundant in liver and serum of animals fed high-fat diet compared with animals maintained on standard chow diet (supplementary Tables III-V).
0.92 Scd1 and Fas in response to high-fat diet, despite increased levels of nSREBP-1c, has, to our knowledge, not been reported previously.
24892698 0.98 Stearoyl-CoA desaturase 1 (Scd1) and Fatty acid synthase (Fasn) genes which encode lipogenic enzymes.
0.98 Fatty Acid Synthase (FAS), which catalyzes formation of fatty acids from acetyl-CoA and malonyl-CoA, as well as Stearoyl Co-A Desaturase 1 (SCD1) which catalyzes the rate-limiting step in the biosynthesis of mono-unsaturated fatty acids used to synthesize triglycerides, is dependent on the activity and expression of the transcription factors Sterol Response Element-Binding Protein (SREBP) 1c and Carbohydrate-Responsive Element Binding Protein (ChREBP).
0.98 Fasn and Scd1 genes is regulated by the transcription factors ChREBP and SREBP1c.
0.98 Scd1 and Fasn.
0.98 Fasn and Scd1 mRNA by 70% and 90% respectively (Fig. 8A and B, gray bars), as expected.
0.98 SCD1 may contribute to the phenotype of Bcl6 KO mice, as Scd1 knockout mice also exhibit reduced adipose tissue mass and decreases in Fasn mRNA expression.
0.98 Fasn and Scd1 gene expression in the liver is mediated by the transcription regulators ChREBP and SREBP1c.
0.98 Fasn and Scd1 expression despite unchanged Srebp1c mRNA levels is consistent with reports that ChREBP can mediate activation of lipogenic gene expression independently of SREBP1c.
0.98 Fasn and Scd1 was also reduced further in both Bcl6 KO and WT mice during fasting, compared to fed mice of the same genotype.
0.97 Fasn or Scd1 gene transcription, even when SREBP gene expression is not changed.
0.97 Fasn, Scd1, or Srebp1c mRNA.
0.97 Fasn, Scd1, and Chrebp was down-regulated rather than increased during Bcl6 deficiency, suggesting that these consequences of Bcl6 deficiency reflect mechanisms indirectly dependent on Bcl6.
0.96 Fasn and Scd1.
0.95 Fasn and Scd1 as in the WT.
0.93 Fasn expression decreased further during fasting, dropping by 65% (Fig. 8A), while Scd1 mRNA (Fig. 8B) decreased by 78% during fasting compared to fed KO.
0.92 Fasn and Scd1 observed in Bcl6 KO mice may be a consequence of reduced food intake, thus resembling fasting.
0.87 Fasn, Scd1, and Chrebp and Srebp1c mRNA (LaPensee, Dent, Schwartz, unpublished).
28327662 0.98 Fasn, Elovl6, Scd1, as well as the transcription factor ChREBP.
0.98 Fasn, Elovl6 and Scd1 through the ChoER sites in their promoters, and Pklr is regarded as a typical target gene of ChREBP.
0.98 Fasn, Scd1 and Elovl6 were markedly increased by ZBTB20 overexpression in the mutant liver (Fig. 4c,d).
0.98 Fasn, Elovl6 and Scd1 were significantly increased by ChREBP-beta overexpression in control liver.
0.98 Fasn, SREBP1c and ChREBP-beta, and to some less extent, of Scd1, Elovl6 and ChREBP-alpha, while Zbtb20 nuclear localization was substantially increased despite of its unchanged mRNA or total protein levels (Fig. 7b-d).
0.98 Fasn, Elovl6 and Scd1, as well as two isoforms of ChREBP.
0.98 Fasn, Elovl6 and Scd1 in the liver.
0.98 Fasn, Elolv6 and Scd1.
0.97 Fasn, Elovl6, and Scd1 were decreased by 42-74% in chow or HCD-fed LZB20KO liver relative to control (Fig. 3b).
0.97 Fasn, Elovl6 and Scd1, without significant effect on Glut5 expression.
0.97 Fasn, Elovl6 or Scd1 in mutant liver, suggesting that ChREBP is required for their expression regulation by ZBTB20.
0.97 Fasn, Elovl6 and Scd1.
0.96 fatty acid synthase (Fasn), elongation of very long chain fatty acids protein 6 (ELOVL6) and stearyl coenzyme A desaturase 1 (SCD1).
0.96 Scd1 in the liver, while no significant binding was detected in the promoters of ChREBP-beta, Glut5, Pklr, Fasn or Elovl6 (Fig. 4a).
0.96 Fasn, Elovl6 and Scd1 in mutant liver, while Glut5 and Gck expression was not changed (Fig. 5a).
0.96 Fasn, Elovl6 and Scd1, while the mRNA expression of Srebp1c and its target Gck was not affected.
0.95 Fasn, Elovl6 and Scd1 are well-established targets of ChREBPs.
28420650 0.98 Fas and stearoyl-CoA desaturase 1 (Scd1).
0.98 Fas and Scd1 were substantially raised (Fig. 1A).
0.98 Fas, and Scd1) and cholesterol efflux (Abcg5 and Abcg8) was markedly increased.
0.98 Fas and Scd1, key enzymes involved in fatty acid biosynthesis, on day 7 of mouse gestation and concurrent early-pregnancy accrual of hepatic triglycerides.
0.98 Fas, and Scd1) suggests reduced hepatic de novo lipogenesis in advanced murine pregnancy.
0.97 fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1), and acetyl-CoA carboxylase 1 (ACC1).
0.97 Fas and Scd1 were not further upregulated in T0901317-fed mice in early pregnancy compared with diet-matched nonpregnant controls (Fig. 2A).
0.97 Fas, and Scd1 was significantly reduced in pregnant mice administered with T0901317 compared with diet-matched nonpregnant controls (Fig. 2A).
0.97 Fas, and Scd1 in the livers of pregnant mice compared with nonpregnant controls (Fig. 3A).
0.97 Fas, and Scd1 as factors involved in the dynamic regulation of triglyceride homeostasis during mouse pregnancy, we aimed to determine whether LXR is involved in control of these adaptations.
0.97 Fas and Scd1 transcription and subsequent triglyceride accumulation.
0.96 Fas, and Scd1 was markedly diminished.
0.96 Fas, Scd1, Acc1, and diglyceride acyltransferase 1 and 2 (Dgat1 and Dgat2)] and cholesterol biosynthetic genes [sterol-regulatory element-binding protein-2 (Srebp2), 3-hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr), and lanosterol 14alpha-demethylase (Cyp51)] in the liver (Fig. 4C).
0.96 Fas, and Scd1 in LXR DKO mice on gestational days 14 and 18.
29057818 0.98 fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD1) and acetyl-CoA carboxylase 1 (ACC1), whose expression is up-regulated by peroxisome proliferator-activated receptor gamma (PPARgamma), CCAAT-enhancer-binding protein alpha (C/BPalpha) and sterol-regulatory element binding protein (SREBP1).
0.98 FAS, SCD1 and ACC1 in hepatocytes.
0.97 FAS, SCD1 and ACC1, while decreasing the expression of HSL in the intramuscular fat tissue.
0.97 FAS and SCD1 were decreased in the zinc-supplemented perirenal adipose tissue.
0.97 FAS and SCD1 are down-regulated in perirenal adipose tissue of chronic zinc-supplemented mice relative to those of control mice, though their gene expression are similar to those of control mice.
0.97 FAS and SCD1 (Figure 6D) may be regulated by chronic high dose zinc supplementation in a post-translational manner.
0.96 FAS (P = 0.0006) was significantly decreased and that of SCD1 (P = 0.0723) tended to decrease in the perirenal adipose tissue of zinc supplemented-mice (Figure 6D and Supplementary Table S16).
0.94 FAS and SCD1 Were Decreased in the Perirenal Adipose Tissue of Chronic Zinc-Supplemented Mice
0.93 FAS and SCD1 decreased or tended to decrease in the perirenal adipose tissue of zinc-supplemented mice, as compared to the control mice.
0.93 FAS and SCD1 in perirenal adipose tissue.
0.92 FAS and SCD1 in adipose tissue remains to be elucidated in further studies.
0.86 FAS and SCD1 remains unchanged in the chronic zinc-supplemented mice.
26035386 0.98 FAS and SCD1.
0.97 fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD1).
0.97 Fasn and Scd1 expression in WT (P<0.05 and P<0.01, respectively), an effect that was more pronounced in IL-6-/- mice (P<0.01 and P<0.001, respectively) (Fig. 3).
0.97 Fasn and Scd1 genes was upregulated after 6 h of the cytokine exposure .
0.97 Fas and Scd1 was downregulated.
0.96 fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD1).
0.96 Fasn (P<0.001) and even Scd1 (P<0.001).
0.96 FAS and SCD1 enzymes was found, which led us to hypothesize that it is a mechanism to compensate for the deficit in fatty acid oxidation.
0.95 FAS and SCD1.
0.95 FAS (P<0.05) and SCD1 (P<0.001) proteins in the IL-6-/- mice fed a HFD and treated with rIL-6, compared with the corresponding HFD-fed group (Fig. 7B).
0.93 FAS and SCD1.
26361872 0.98 FAS, stearoyl-CoA desaturase-1 (SCD1), and Lipin1 are likely contributing to reduced SERCA activity in mdx mice.
0.98 FAS, SCD1, and Lipin1 that coincided with a disrupted phospholipid composition of the SR membrane bilayer.
0.98 FAS, SCD1, and Lipin1 in mdx myocytes rescued reduced SERCA-dependent Ca2+ uptake, suggesting that dysregulated lipogenesis might contribute to aberrant Ca2+ metabolism in muscular dystrophy.
0.97 FAS, SCD1, and Lipin1 (triple transgenic, or 3TG) had an additive effect, restoring ~60% of SERCA's function in mdx myotubes (Figure 4A, 8th bar, Mdx + 3TG).
0.97 FAS, SCD1, and Lipin1 in mdx myotubes had a robust effect on SR phospholipidome.
0.97 FAS or Lipin1 knockdown was sufficient to promote lower SERCA-dependent Ca2+ uptake in WT myocytes, and restoration of FAS, SCD1, and Lipin1 had cumulative effects on rescuing compromised SERCA function in mdx myocytes.
0.96 FAS, SCD1 and Lipin1 (3TG) in mdx myocytes partly rescued SERCA activity, which coincided with an increase in SR PE that normalized PC/PE ratio.
0.95 FAS, SCD1, Lipin1, CEPT1), or ER-associated organelles such as lipid droplets that are derived from ER (HSL, ATGL, and Plin2) and mitochondria-associated membranes that traffic molecules between ER and mitochondria (PSS2).
0.91 FAS, SCD1 and Lipin1 does not entirely explain the altered SR phospholipidome in mdx myotubes.
0.89 FAS and SCD1 were ~7-fold lower in mdx muscles compared to WT controls.
0.78 FAS, SCD1, Lipin1, or 3TG expression in WT myotubes had no effect on SERCA-dependent Ca2+ uptake (Figure 4D-E).
20218765 0.98 SCD1 LKO mice is likely be due to impaired lipogenesis in response to carbohydrate feeding, as a reduction in expression of SREBP-1c and its downstream target genes involved in DNL including ACC, FAS, and ELOVL6 was observed.
0.98 SCD1, FAS and Elovl6, infusion of triglyceride:palmitoleate reduced the expression of these genes.
0.97 FAS, stearoyl-CoA desaturase (SCD), and glyceraldehyde-3-phosphate acyltransferase (GPAT) (Figure 2) (; Horton et al.,).
0.96 FAS and SCD1, respectively, enzymes that catalyze rate-limiting steps in the synthesis of saturated and monounsaturated fatty acids, respectively, that are commonly incorporated into other complex lipid species as well.
0.96 SCD1 LKO mice, however, was a reduction in expression of lipogenic genes including SREBP-1c, FAS, and ACC after ten weeks of ASO treatment.
0.96 SCD1 SKO, other lipogenic genes including ACC and FAS were expressed at comparable levels to Lox controls.
0.93 fatty acid synthase, fatty acid elongase 6, and stearoyl-CoA desaturase 1.
0.87 FAS, ELOVL6, and SCD1, future experiments will likely yield many additional insights into the regulation of metabolism, lipogenesis and diet-induced obesity and how these enzymes mediate these metabolic processes.
0.61 SCD1 ASO treatment reduced hepatic ACC but not FAS, and an impact of ASO treatment on lipogenesis was not conclusively demonstrated although liver triglycerides significantly increased.
26120082 0.98 FASN, and SCD1.
0.98 FASN, SREBP1-c, and SCD1 (Figures 3F and 3G).
0.97 fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD1), and acetyl-CoA carboxylase-1 (ACC1) acting downstream of glycolysis.
0.97 FASN, SCD1, and ACC1 as well as the sterol-regulatory element binding protein-1c (SREBP1c), a transcription factor that regulates lipogenic gene expression, is associated with numerous forms of cancer.
0.97 FASN, ACC1, SCD1, and SREBP1c activity have been shown to reduce proliferation and induce apoptosis in cancer cells.
0.97 SCD1, FASN, and SREBP1c) enzyme expression in colon tumor xenografts (Figures 4D and 4E).
0.96 SCD1, and FASN expression was markedly suppressed (Figures 5C-5E).
0.93 FASN and SCD1 (Figure S3D) and intriguingly did not inhibit the expression of SREBP1c in normal cell lines in contrast to the profound effect on SREBP1c expression observed in cancer cells (Figures S3D and 3G).
0.92 FASN, and SCD1 in cancer cells treated with SR9243 (10 muM) for 6 hr.
27121981 0.98 fatty acid synthase (FAS), acyl-CoA carboxylase (ACC), and stearyl-CoA desaturase-1 (SCD1).
0.97 FAS, SCD1, and ACC, was dramatically upregulated 3.4-, 13.1- and 4.7- folds, respectively, compared with control mice.
0.97 FAS and SCD1 (Fig. 4A,B).
0.97 FAS and SCD1 were largely diminished by GPR40 knockdown (Fig. 4C).
0.97 FAS, SCD1, and ACC stimulated by LXR.
0.96 FAS, SCD1 and ACC, and then increased lipid accumulation in the livers of mice.
0.96 FAS, SCD1, and ACC induced by LXR and further suppressed lipid accumulation in the livers of mice and HepG2 cells via AMPK pathway.
0.92 FAS, SCD1, and ACC, respectively, compared with HCD-fed plus vehicle-treated mice (Fig. 2A).
0.87 FAS, and SCD1, respectively, and 2.6- and 2.5- fold increase in protein levels for FAS and SCD1, respectively.
28326002 0.98 FAS, and stearoyl-CoA desaturase-1 (SCD-1) was also down-regulated by SV10E.
0.98 FAS, SCD-1, and fatty acid translocase (CD36) (Figure 6).
0.98 FAS, and SCD-1, leading to morphological changes and lipid accumulation in cells.
0.98 FAS and SCD-1.
0.98 FAS, SCD-1, and SREBP-1c were markedly suppressed following SV10E treatment (Figure 7(b)).
0.98 FAS and SCD-1 are the central lipogenic proteins that, along with CD36, which is an integral membrane protein importing fatty acids inside cells, contribute to energy storage by increasing fatty acid uptake in the liver.
0.97 FAS, SCD-1, SREBP-1c, and CD36 in white adipose tissue and liver were suppressed by SV10E administration.
0.97 FAS, SCD-1, and CD36.
0.96 FAS and SCD-1, which are the key enzymes in fatty acid metabolism responsible for synthesizing palmitate (C16:0) from acetyl-CoA and forming a double bond in stearoyl-CoA, were also reduced by administration of SV10E.
28671595 0.98 FAS, SCD-1, and fatty acid translocase (CD36), compared with HFD in the hepatic tissue (Figure 5).
0.98 FAS and SCD-1.
0.97 FAS, SCD-1, and CD36, in epididymal adipose tissue and hepatic tissue.
0.97 FAS and SCD-1.
0.96 FAS and SCD-1 are the key enzymes involved in fatty acid metabolism responsible for synthesizing palmitate (C16:0) from acetyl-CoA and forming a double bond in stearoyl-CoA. However, VDAE administration reduced the expressions of these genes, including PPAR-gamma, C/EBP-alpha, aP2, FAS, and SCD-1.
0.96 FAS, SCD-1) and hepatic lipid metabolites (fatty acids, phospholipids, lipid moieties) were clearly suppressed by VDAE administration in hepatic tissue.
0.96 FAS, SCD-1, and CD36.
0.92 FAS and SCD-1, were also reduced by VDAE.
0.88 fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) and fatty acid esterification transcriptional factors, such as stearoyl-CoA desaturase (SCD-1), is important in the process of lipogenesis in adipose and hepatic tissues.
31952262 0.98 SCD-1, FAS, ACC and GPAT through the insulin signaling pathway.
0.98 FAS, and SCD-1.
0.98 FAS, SCD-1, ACC1.
0.97 FAS, ACC1, and SCD-1 protein levels in the liver.
0.96 FAS, SCD-1, ACC1, and HMGCR.
0.93 FAS, ACC, SCD-1.
0.82 FAS, ACC, and SCD-1 in the HFD + Scr ODN group were significantly higher than those in the NC and SREBP ODN group.
0.81 fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA desaturase (SCD)-1, and carbohydrate response element binding protein (ChREBP) were measured in hyperlipidemic liver tissue by western blot analysis (Figure 4B,C).
0.67 FAS, and SCD-1, in the liver were measured by western blot analysis.
27298813 0.98 fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1), and acetyl-CoA carboxylase 1 (ACC1), which promotes de novo fatty-acid synthesis.
0.98 SCD1, ACC1 and FAS, which promote de novo fatty-acid synthesis.
0.98 FAS, SCD1 and ACC1.
0.97 SCD1, ACC1 and FAS.
0.96 FAS, SCD1 and ACC1.
0.90 FAS, SCD1 and ACC1 mRNA expression as compared with silymarin at 250 mg/kg.
0.77 SCD1, ACC1, FAS, PPARgamma and DGAT2), decreases mRNA expression of genes involved in fatty acid oxidation (PPARalpha, ACO and CPT1) or master transcription factor of antioxidant gene (Nrf2) were observed with histopathological changes related to hepatosteatosis (noticeable increases of the percentages of changed fatty regions, the number of changed fatty hepatocytes and mean hepatocyte diameters) and increases of NT and 4-HNE-immunolabelled hepatocytes, following continuous oral administration of EtOH for 2 weeks in the present study.
0.74 SCD1, ACC1, FAS, PPARgamma and DGAT2 in the present study.
28704726 0.98 FASN and SCD1.
0.98 FASN and SCD1, which are involved in de novo synthesis of saturated and unsaturated long-chain FFAs.
0.97 FASN and SCD1 by hypoxia were reversed by silencing BNIP3 expression (Fig. 5C and D).
0.96 FASN inhibition by cerulenin (a FASN inhibitor) but not by CAY10566 (a SCD1 inhibitor) increased apoptosis of UCB-hMSC exposed to hypoxia (Fig. 5E).
0.96 FASN, not by SCD1.
0.88 FASN and SCD1 regulated by BNIP3 in apoptosis and migration of UCB-hMSCs under hypoxia.
0.72 FASN, stearoyl-CoA desaturase 1 (SCD1), SCD5, glycerol-3-phsphate acyltransferase 1 (GPAT1), GPAT3, GPAT4, monoacylglycerol lipase (MAGL), diglyceride acyltransferase 1 (DGAT1), and carnitine palmitoyltransferase 1A (CPT1A) in UCB-hMSCs under hypoxia.
0.64 FASN and SCD1 regulated by BNIP3 in migration induced by hypoxia pretreatment and survival under hypoxia in UCB-hMSCs.
22682225 0.98 fatty acid synthase (Fasn) and stearoyl CoA desaturase 1 (Scd1), showed a similar expression pattern with Acc, Fasn and Scd1 increased two- to ten-fold in both control and LIRKO mice (Fig. 1B-D).
0.96 Scd1, Acc and Fasn in both control and LIRKO mice (Fig. 5J).
0.94 Scd1, Acc, Fasn and pyruvate kinase increased three- to tenfold with fructose feeding.
0.93 Scd1 was increased 20-fold and Acc, Fasn and pyruvate kinase were increased five- to ten-fold with fructose feeding.
0.91 Fasn (Fig. 6F), and an eight-fold induction in Scd1 (Fig. 6G).
0.87 Fasn and Scd1(Fig.
0.72 Fasn and Scd1 was similar in wildtype and ob/ob mice.
24067358 0.98 fatty acid synthase (FAS) and stearoyl-CoA desaturase1 (SCD1), compared with the HF/HS-fed group (Fig. 4).
0.98 FAS, SCD1, and other enzymes regulating hepatic lipogenesis, and produces a pronounced elevation of hepatic TG concentrations with an increase in plasma TG.
0.98 FAS and SCD1 in the liver.
0.98 FAS and SCD1 is regulated by SREBP-1c at the transcriptional level.
0.98 FAS and SCD1).
0.97 FAS and SCD1.
0.82 FAS and SCD1) and fatty acid metabolism (ACO and MCAD) in the liver of C57/BL6J mice fed diets containing HF/HS and Yabukita 1% or Benifuuki 1% extract powders.
24425205 0.98 fatty acid synthase (FASN), acetyl-CoA carboxylase1 (ACC1), steroyl-CoA desaturase1 (SCD1), and long-chain fatty acid elongase (ELOVL6).
0.98 FASN, ACC1, and SCD1, is also modulated in a fashion analogous to that of nutritionally regulated SREBP1c.
0.98 FASN, SCD1, ACC1, and ELOVL6 (Fig. 4C, lane 2).
0.98 FASN, SCD1, and ELOVL6 in primary hepatocytes (Fig. 4C, lane 3).
0.97 FASN, and SCD1 were decreased by forskolin, whereas RNF20 suppression by way of siRNA restored the expression of lipogenic genes, even in the presence of forskolin (Fig. 6E).
0.97 FASN, SCD1, and ELOVL6 was significantly attenuated in the liver of RNF20-overexpressing mice (Fig. 7D).
0.97 FASN, and SCD1 were increased in the liver of insulin-resistant mouse models, the level of hepatic RNF20 was not significantly altered (Supporting Fig. S8A,B).
30201876 0.98 Fas, and Scd.
0.98 FAS and SCD-1, as well as aP2, which is a fatty acid carrier protein.
0.97 Fasn, Acac-beta, Srebf-1, and Scd1 compared to the ND group (Figure 5A-E).
0.96 fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl-CoA desaturase (SCD-1)), and a transcriptional factor involved in fatty acid esterification was controlled by a sterol regulatory element-binding protein (SREBP-1).
0.96 Fas, and Scd1, was effectively suppressed by a higher dosage of SLT.
0.94 SCD-1 is a key molecule, implicated in the process of acetyl-CoA to synthesize palmitate (C16:0), and forms a double bond in stearoyl-CoA. A recent study has evidently reported that the supplementation of the herbal extract of Valeriana dageletiana lowered the expression of genes involved in lipogenesis such as Srebp1, Fas, and Scd1.
0.92 Fasn, (C) Acac-beta, (D) Srebf1, and (E) Scd1 in the liver tissue of HFD C57BL/6 mice.
21471514 0.98 FAS, and SCD1) when combined with an active glucose flux in vivo.
0.98 FAS, and SCD1) was significantly decreased (Fig. 6C).
0.98 FAS, and SCD1) when combined with an active glucose flux in vivo.
0.98 FAS, and SCD1 genes were described as synergistically regulated by ChREBP and SREBP-1c, we report here that the stimulatory effect of OGT on lipogenic genes is highly dependent on ChREBP activity (Fig. 5).
0.97 FAS, and SCD1 gene expression was measured in refed GFP mice:an increase that was significantly potentiated in the liver of refed OGT mice (Fig. 4A).
0.97 FAS, and SCD1 gene expression was further increased in OGT-overexpressing hepatocytes compared with GFP cells.
21711241 0.98 Fasn (fatty acid synthase), Scd1, Scd2 (stearoyl-Coenzyme A desaturase 1 and 2), and Elovl6 (long chain fatty acid elongase 6).
0.98 Scd1, Fasn, and Ucp1 (Fig. 6A).
0.98 Scd1 and Fasn on heart sections of untreated and ranolazine-treated B6 mice with 6 months of AAC confirmed the down-regulation of key fat synthesizing enzymes by ranolazine (Fig. 6, upper and middle panels).
0.98 Fasn, Scd1 and Ucp1 (Fig. 7B).
0.96 Fasn, Scd1 and Ucp1 protein levels on heart sections of cystamine-treated ApoE-/- mice compared to untreated ApoE-/- and B6 mice (Fig. 7C).
0.93 Scd1 and Fasn protein levels in heart tissue of aged ApoE-/- mice (Fig. 6D, upper and middle panels).
22721968 0.98 Scd1, and Fasn are activated by sterol regulatory element-binding protein-1c (SREBP-1c), which is a transcription factor and master regulator of lipogenesis.
0.98 SCD1 and FAS mRNA levels, as well as protein levels of GPAT1, SCD1, and FAS, and GPAT-mediated TG/diacylglycerol (DG) biosynthesis were increased in the adult liver relative to the neonatal liver (Fig. 1A and Supplementary Fig. 2).
0.97 SCD1 and FAS are involved in fatty acid biosynthesis, the differential positioning of GPAT1, SCD1, and FAS in the TG biosynthesis pathway may explain the different mechanisms of their gene expression.
0.95 Scd1 and Fasn promoters (Fig. 4C), in Dnmt3b-expressing hepatocytes relative to control GFP-expressing hepatocytes.
0.92 Scd1 and Fasn transcription is regulated in the neonatal liver.
0.89 Scd1 and Fasn promoters, containing SREs, was not observed in both the neonatal (day 0) and adult (10 weeks of age) livers (Fig. 1E).
26346310 0.98 FAS, and SCD1).
0.97 fatty acid synthase (FAS), stearoyl-CoA desaturase (SCD1), and sterol regulatory element-binding protein 1c (SREBP1c) were downregulated, while lipolytic gene carnitine palmitoyltransferase-1 (CPT1) was upregulated in BBR-SLN-treated livers.
0.97 SCD1, FAS, and SREBP1c in the liver were significantly downregulated, while the CPT1 mRNA level was increased compared to the control mice (P<0.05).
0.97 SCD1, FAS, and SREBP1c expression (P<0.05) following the downregulation of SCD1 and FAS, which suggested that the increased hepatic expression of SREBP-1c might lead to fatty liver and increase rate of hepatic fatty acid synthesis with an increase in lipogenic genes like FAS, ACC, and SCD.
0.96 FAS, ACC, and SCD1 are key enzymes controlling the lipogenic pathway.
0.96 SCD1, and FAS expression.
27867269 0.98 FAS, SCD-1, LPL, and Adiponectin.
0.98 SCD-1 and FAS [Figure 5A], the target genes of SREBP1c, by BPP during adipocyte differentiation imply that the inhibition of adipogenesis is mediated by the regulation of lipogenesis.
0.98 FAS and SCD-1.
0.98 FAS and SCD-1during adipocyte differentiation and these results indicate that inhibition of adipocyte differentiation can be mediated by the down-regulation of these lipogenic genes.
0.97 SCD-1, FAS, aP2 and LPL.
0.97 SCD-1, FAS, aP2 and LPL.
29371918 0.98 fatty acid synthase (FAS), SCD-1 & CD36 that are involved in lipid partitioning, poly-unsaturated fatty acids (PUFA) synthesis and influx of fatty acids in hepatocytes, and these were elevated in liver tissues of FF diet fed mice.
0.98 FAS and SCD-1, while there was also decreased influx and transport of fatty acids as TC & EV treatments prevented CD36 up-regulation in mice and in AML-12 cells exposed to palmitate (Figure 6).
0.97 FAS (p<0.0001), SREBP1 (p<0.0001) & SCD-1 in palmitate treated cells (Figure 4B, 4C, 4D, 4E).
0.97 FAS, SCD-1 & CD36.
0.89 FAS were increased by 8 and 6.9 fold respectively (p<0.001), while m-RNA levels of SREBP1 & SCD-1 were significantly increased by 1.4 & 1.5 fold respectively as compared to non-treated control cells (Figure 4B, 4C, 4D, 4E).
0.84 Scd-1 (### indicates p<0.001, TC versus FF group, EV versus FF group), Srebp1 (# indicates p<0.05, TC versus FF group, EV versus FF group), PPAR-y and Fas (## indicates p<0.01, TC versus FF group, ### indicates p<0.001, EV versus FF group).
19966778 0.98 SCD-1 and Fasn are direct transcriptional targets of the nuclear receptor LXR (LXR-responsive elements, LXRE, are located on Fasn, between positions -669 and -665, and SCD-1, between positions -1263 and -1248) (Fig.6a).
0.98 Fasn and SCD-1 mRNA levels, demonstrating that LXR-alpha is mainly responsible for the upregulation of these genes in the absence of aP2 (Fig.6d and Supplementary Fig.5e).
0.98 Fasn and SCD-1 transcription and resistance to lipotoxic ER stress and identified the transcriptional mechanism underlying this function of aP2.
0.97 Fasn and SCD-1 was also markedly down-regulated in aP2-/-Nr1h3-/- macrophages compared to aP2-/- cells (Supplementary Fig.6b,c).
0.76 Fasn and SCD-1 promoters.
20227267 0.98 fatty acid synthase (FAS) and stearoyl CoA desaturase (SCD1).
0.98 FAS and SCD, has been recognized for some time.
0.97 FAS and SCD1.
0.97 FAS (but not SCD) mRNA to a greater extent than SREBP1c.
0.82 FAS and SCD expression in the hamster are very different from those in the mouse.
23465594 0.98 FASN, SCD-1 and ELOVL6.
0.97 Fatty acid synthase (FASN) catalyzes the production of saturated fatty acids such as palmitate from malonyl CoA and palmitate is converted to stearate via fatty acid elongases such as ELOVL6 and desaturated via stearoyl CoA desaturase-1 (SCD-1).
0.97 SCD-1, ATP citrate lyase (ACLY) and FASN.
0.97 Scd1, FASN, ACLY, ELOVL2, ELOVL3 and ACC expression.
0.89 FASN, ACC) or downregulation of mRNA expression (Scd1, ELOVL5) following chronic ethanol administration.
23999723 0.98 stearoyl coenzyme A desaturase 1 (SCD-1), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) expression, target genes of SREBP1c.
0.98 SCD-1, FAS, and ACC (Figure 6C), the target genes of SREBP1c, by 1 during adipocyte differentiation imply that the inhibition of adipocyte differentiation is mediated by the regulation of lipogenesis.
0.98 SCD-1, ACC, and FAS, the target genes of SREBP1c.
0.98 SCD-1, ACC, and FAS) by treatment with 1 during adipocyte differentiation implies that inhibition of adipocyte differentiation can be mediated by the down-regulation of these lipogenic genes.
0.98 SCD-1, ACC, and FAS, affecting from early stage to terminal stage of adipogenesis.
24722245 0.98 fatty acid synthase (FAS), stearoyl CoA desaturase 1 (SCD1), acetyl CoA carboxylase 2 (ACC2), and peroxisome proliferator-activated receptor gamma (PPARgamma) in MKP-3-/- mice fed an HFD compared with WT mice fed an HFD (Fig. 2E).
0.98 FAS, and SCD1 (Fig. 4F).
0.98 FAS, SCD1, and ACC2 genes (Fig. 7A).
0.96 FAS, SCD1, and ACC2 genes at 5 nmol/L (Fig. 7B).
0.94 FAS, and SCD1 (Fig. 4E).
24857376 0.98 fatty acid synthase (Fas), acetyl-CoA carboxylase (Acc), and stearoyl-CoA desaturase 1 (Scd1).
0.98 Fas, Acc, Scd1, and SREBP-1c.
0.98 Fas, Acc, Scd1, malic enzyme, ATP-citrate lyase, and glycerol-3-phosphate acyltransferase (Gpat) were lower in ob/ob-Ppargamma H livers than in those of ob/ob-PpargammaWT mice, suggesting that PPARgamma promotes the development of fatty liver in ob/ob mice by upregulating the expression of lipogenic genes.
0.98 Fas, Scd1, and Gpat.
0.96 Fas, Scd1, and Gpat mRNAs, known hepatic LXRalpha-SREBP-1c and PPARgamma targets, in PpargammaWT and Ppargamma H mice with an OB/OB or ob/ob genetic background.
25156247 0.98 Fas and Scd-1.
0.98 Scd-1 and Fas.
0.98 Scd-1 and Fas upon administration of a synthetic LXR agonist contributes to massive hepatic steatosis in mice.
0.98 Scd-1 and Fas under control diet.
0.98 Scd-1 and Fas.
26856717 0.98 FAS and SCD1 can be induced by fructose feedings even in mice with liver specific knockout of insulin receptor, indicating that fructose can stimulate lipogenesis in the setting of a complete lack of insulin signaling.
0.97 FAS, and SCD1.
0.95 FAS, SCD1 and ELOVL6 has been studied extensively in mice, both as global and liver-specific knockouts.
0.93 FAS and SCD1 than HFD.
0.91 FAS, and SCD1 in liver, but these mice eventually developed NAFLD after 12 weeks.
30274245 0.98 Fasn, Acly, Acc1, Scd1, and Elovl6, and adipocyte differentiation such as Pparg2, Cebpa, and Fabp4.
0.98 fatty acid synthase (FASN), stearoyl-CoA desaturase-1 (SCD1), and ChREBP-beta.
0.97 FASN, ACC1, and stearoyl-CoA desaturase-1 (SCD1).
0.97 Fasn, Acc1, and Scd1 were up-regulated in BAT.
0.97 FASN-mediated synthesis of palmitate, followed by SCD1-catalyzed desaturation.
30618759 0.98 FASN, SCD-1 and glycerin-3-phosphate acyltransferase (GPAT).
0.97 FASN, and SCD1 in hypercholesterolemic mice, suppressing the synthesis of fatty acids in liver.
0.96 FASN, and SCD1 in the liver, so suppressed the synthesis of fatty acid and lowered plasma lipid levels.
0.95 fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD-1), sterol regulatory element-binding protein (SREBF) in liver in high fat diet feeding ApoE-/- mice.
0.92 FASN, SCD-1, sterol regulatory element-binding protein (SREBF) in liver in high fat diet feeding ApoE-/- mice (Figure 7A), consistent to this, FASN and SCD-1 protein level showed a decrease in mice treated with leonurine (Figure 7B), thereby reducing the synthesis of fatty acid in liver, so help to reduce blood lipid levels.
30739427 0.98 fatty acid synthase and stearoyl-CoA desaturase were highly expressed in the skin and livers of the db/db mice.
0.98 SCD were noted in the skin of db/db mice compared with db/m mice, whereas LXRalpha/beta, PPARgamma, Elovl6, FAS, and SCD were significantly higher in the livers of db/db mice, indicating a profound change in both lipid metabolism and synthesis in both the skin and livers of db/db mice.
0.98 FAS, and SCD) were upregulated in the skin and livers of db/db mice, suggesting that lipid synthesis is stimulated both peripherally and centrally in db/db mice.
0.98 FAS, and SCD also receive positive regulation from lipid metabolites and nuclear receptors, including LXR and PPARgamma, which explains how their higher expression in db/db mice could contribute to the enrichment of lipids in the skin and liver.
0.93 FAS and SCD also play critical roles in the synthesis of fatty acids, producing a saturated fatty acid, palmitic acid (C16:0), from acetyl-CoA and malonyl-CoA and forming monounsaturated fatty acids respectively.
30884812 0.98 Fasn (p = 0.006), Scd1 (p < 0.001) and Lpl (p < 0.001) in comparison with DMSO-control cells.
0.98 Scd1, Fasn and Lpl by resveratrol treatment demonstrates the potent inhibitory activity of this polyphenol on both adipogenesis and lipogenesis processes.
0.97 Fasn, Lpl or Scd1, which constitute key regulators of the fatty acid metabolism, triglyceride uptake and lipid storage.
0.97 Fasn (p = 0.017), Lpl (p = 0.016) and Scd1 (p = 0.030).
0.92 Scd1, Fasn and Lpl.
31083413 0.98 fatty acid synthase (Fas), acetyl-CoA carboxylase 1 (Acc1), stearoyl-CoA desaturase-1 (Scd1), Scd2, glycerol-3-phosphate acyltransferase (Gpam), diacylglycerol O-acyltransferase 1 (Dgat1), and Dgat2, were significantly reduced in arazyme-treated mice (Figure 3A-C).
0.98 Fas, Acc1, Scd1, Scd2, Gpam, Dgat1, and Dgat2.
0.97 Fas, Acc2, Scd1, Scd2, Gpam, Dgat1, and Dgat2.
0.97 FAS protein levels, as well as SREBP-1 target gene mRNA levels, including Fas, Acc1, Scd1, Scd2, Gpam, Dgat1, and Dgat2, inhibiting hepatic fatty acid and TG synthesis.
0.95 fatty acid synthase (Fas), acetyl-CoA carboxylase 1 (Acc1), stearoyl-CoA desaturase-1 (Scd1), Scd2, glycerol-3-phosphate acyltransferase (Gpam), diacylglycerol O-acyltransferase 1 (Dgat1), and Dgat2.
31729980 0.98 SCD1, FAS, ACC1, GPAM and DGAT2 in mouse liver.
0.98 fatty acid synthase (FAS), acetyl CoA carboxylase 1 (ACC1) and stearoyl-CoA desaturase 1 (SCD1).
0.98 SCD1, FAS, and ACC1) were increased, and the expression of genes involved in TG synthesis (GPAM and DGAT2) was increased markedly (Fig. 4d).
0.98 SCD1, FAS, and ACC1), without significantly influencing CD36, PPARalpha and MTTP expression (Fig. 5a).
0.98 SCD1, FAS, ACC1, GPAM and DGAT2).
18805087 0.98 FAS, SCD-1, and ELOVL6, the three principal enzymes that mediate de novo fatty acid synthesis, in adipose tissues of FABP-/- mice (Figure 6A).
0.97 SCD-1, fatty acid synthase (FAS) and fatty acid elongase 6 (ELOVL6) expression in liver compared to vehicle-infused mice.
0.97 SCD-1 and FAS promoter activities (Figure 6B).
0.95 FAS and coordinated regulation of SCD-1.
23964317 0.98 SCD1 and FAS) in de novo lipogenesis.
0.98 SCD1 and FAS).
0.94 stearoyl-CoA desaturase 1 (SCD1), and fatty acid synthase (FAS), which promote synthesis of de novo monounsaturated fatty acid, were significantly lower in both the 0.01% (w/w) CA and 0.02% (w/w) CA diet groups, than in the HFD group (Fig. 5A, P < 0.05).
0.77 stearoyl-CoA desaturase 1 (SCD1), and fatty acid synthase (FAS), was significantly lower in mice fed 0.01% (w/w) CA and 0.02% (w/w) CA diets than that in the HFD group; on the other hand, the expression level of beta-oxidation-related genes, such as peroxisome proliferator-activated receptor alpha (PPAR-alpha), carnitine palmitoyltransferase 1 (CPT-1), and acyl-CoA oxidase (ACO), was higher in mice fed a 0.02% (w/w) CA diet, than that in the HFD group (P < 0.05).
27333268 0.98 Fas and Stearoyl-CoaA desaturase (Scd1) was no longer up-regulated by IL-6 in the presence of siRNA Stat3 in hepatocytes, therefore indicating that IL-6-mediated signalling promotes the expression of these enzymes via activation of Stat3.
0.97 Fas enzymes was observed in samples from mice fed a HFD and treated with rIL-6, and levels of the Scd1 enzyme were further reduced (Fig 3B).
0.96 Fasn levels, but a significant decrease (P<0.01) in Scd1 expression as compared with the levels found in the STD condition (Fig 3A).
0.80 Fas levels, except for that of Scd1 which was reduced (P<0.001) compared with the STD group (Fig 3B).
27846372 0.98 Fasn and Scd1, we inferred that SCD1 activity was the major regulator of NR1H/LXR-induced LD accumulation in response to PA (Fig. S3A, B).
0.97 Scd1 and Fasn in the presence of PA (Fig. 1F).
0.95 Scd1 and Fasn but had only a moderate effect on Srebf1 (Fig. 3C-E).
0.83 Scd1, we analyzed the expression of several other NR1H/LXR target lipogenic genes such as Fasn and Srebf1/Srebp1c.
28732092 0.98 Fasn (Fatty acid synthase) or Scd1 and directly promote de novo fatty acid synthesis.
0.98 Fasn, Elovl6 and Scd1 in an LXR dependent manner (Fig 3A).
0.96 Fasn, Scd1, Srebp-1c and Chrebp promoters.
0.95 FASN, ELOVL6 and SCD1) (Fig 3B: S1 Fig).
30218046 0.98 FASN, ELOVL5, and SCD1 activity is inhibited by a complex of PPARA and PPARGC1A with LPIN1 and 2, which had lower expression in SPF mice in our experiments (Fig. 3c).
0.97 FASN, SCD1, and ELOVL6, which catalyze the synthesis of saturated fatty acids (SAFA) and MUFA from acetyl-CoA; and SC5D and LSS, which are involved in cholesterol biosynthesis.
0.89 Fatty acid synthase (FASN) catalyzes the generation of palmitate (FA 16:0) from acetyl-CoA. FA 16:0 can be further metabolized by stearoyl-CoA desaturase 1 (SCD1) and long chain fatty acid elongase 6 (ELOVL6).
0.83 FASN (Fig. 3a); (II) Delta-9 desaturation of palmitate (FA16:0) to palmitoleate (FA16:1 n-7) by SCD1 (Fig. 3a); (III) Elongation of FA18:3 n-6 to FA20:3 n-6 by ELOVL5 (Fig. 3b), with higher values for SPF in all steps.
31270932 0.98 SCD1, FAS, SREBP2 and HMGCR, and up-regulated glycogen synthesis proteins, including Akt2 (Ser474) phosphorylation, GLUT2 and GSK-3beta, in the liver of obese mice.
0.98 FAS and SCD1.
0.97 FAS and SCD1 expression.
0.97 FAS, SCD-1, SREBP and HMGCR are important metabolic enzymes in the liver.24, 25, 26, 27 After we knocked down the FAIM with LV-shFAIM, the levels of these lipogenesis enzymes elevated, but declined in the LV-FAIM mouse liver tissue.
31558861 0.98 SCD1 and FAS (Figure 2A).
0.98 SCD1, FAS and acetyl-CoA carboxylase (ACC), in PA-treated AML-12 cells (Figure 5A).
0.98 SCD1 and FAS, and increased expression of fatty acid beta-oxidation genes, including PGC1alpha, PPARalpha and CPT1alpha.
0.84 stearoyl coenzyme A desaturase 1 (SCD1), fatty acid synthase (FAS) and acetyl-CoA carboxylase 1 (ACC1), were determined.
31936890 0.98 fatty acid synthase (FAS), stearoyl-coenzyme A desaturase 1 (SCD-1), acetyl-coenzyme A carboxylase (ACC), and fatty acid translocase (FAT).
0.98 FAS, FAT, ACC, SCD-1, and SREBP-1c mRNA in MDI-treated cells increased significantly compared to the undifferentiated cells.
0.98 FAS, FAT, ACC, SCD-1, and SREBP-1c genes, known as adipokines or adipogenic genes.
0.95 FAS, FAT, ACC, and SREBP-1c mRNA expression in MDI-treated cells, but treatment with 20 muM ergosterol peroxide did not suppress SCD-1 mRNA expression.
32257945 0.98 FAS and SCD-1.
0.98 FAS (Figure 7B) and SCD-1 protein expression (Figure 7C) in HFD mice (both vehicle- and doxorubicin-treated) within mammary adipose tissue, which translate to a decrease in lipogenic activity in mammary adipose tissue of the HFD (obese) animals.
0.96 SCD-1 and FAS expression was higher in the LFD mice, irrespective of treatments, as dietary carbohydrates are substrates for de novo FA synthesis.
0.92 Fatty acid synthase (FAS) and sterol CoA-desaturase-1 (SCD-1) were found to be significantly decreased in the vehicle-H mice, compared to vehicle-L mice (FAS, p < 0.01 and SCD-1, p < 0.01 Figures 7B,C) and Dox-H mice compared to Dox-L mice (FAS, p < 0.01, and SCD-1, p < 0.01 Figures 7B,C), respectively.
19166967 0.98 fatty acid synthase (FAS; Fasn) and Scd1 (Figure 1).
0.97 SCD1 is downstream of FAS and converts FAS-derived saturated fatty acids into MUFA, it is possible that impaired hepatic MUFA synthesis is responsible for many of the metabolic phenotypes elicited by hepatic deficiency of either SCD1 or FAS.
0.97 SCD1 catalyzes the conversion of the saturated fatty acid products of FAS into MUFA, which are the preferred substrate for triglyceride synthesis.
21178610 0.98 FASN, SCD1 and Elovl6) involved in DNL and MUFA synthesis.
0.97 FASN) and MUFA synthesis (SCD1 and Elovl6) synthesis are coordinately controlled during fasting and refeeding, and by insulin, dietary carbohydrate and dietary fat (Fig. 1).
0.95 fatty acid synthase (FASN) or MUFA synthesis, that is, stearoyl CoA desaturase-1 (SCD1) or fatty acid elongase-6 (Elovl6), significantly affects the severity of diet-induced hyperglycemia, dyslipidemia and fatty liver.
21869929 0.98 fatty acid synthase (FASN), and stearoyl CoA desaturase-1 (SCD1) (Table 2).
0.96 FASN, and SCD1, reduces glucose and FA uptake by reducing GLUT4 and LPL expression, increases FA oxidation by increasing CPT1 and UCP2 expression and reduces adipocyte proliferation and differentiation by reducing PPAR-gammaand its downstream genes.
0.95 FASN, and SCD1) genes in the absence of insulin in mice fed trans-10, cis-12 CLA further supports this argument.
26476289 0.98 fatty acid synthase (FASN), and stearoyl-CoA desaturase 1 (SCD1).
0.97 FASN, either alone or in association with N-Ras, c-Met or SCD1, is not sufficient to malignantly transform hepatocytes and drive liver tumor development.
0.73 FASN transfection was unable to drive tumor development or lipid accumulation in the mouse liver when co-injected with another lipogenic enzyme, SCD1 (Fig. 1D; n=5).
29520981 0.98 FAS and SCD1.
0.97 FAS and SCD1, both of which are involved in lipid metabolism, were significantly downregulated in both the LC with Tofo and the SR diet alone groups.
0.66 FAS, SCD1 and unsaturated fatty acids, our results revealed different outcomes in terms of glucose and lipid metabolism.
29890650 0.98 FASN are two key enzymes involved in lipogenesis, helping acetyl-CoA to form palmitic acid desaturated by SCD1.
0.97 fatty acid synthase (FASN), acetyl-CoA carboxylase-1 (ACC1), and stearoyl-coenzyme desaturase-1 (SCD1) and increase carnitine palmitoyl transferase 1 (CPT1) level to regulate lipid metabolism.
0.94 FASN (fatty acid synthase), and SCD1 (stearoyl-coenzyme A desaturase 1), and improved CPT1 (carnitine palmitoyltransferase 1) level by activating FXR to regulate lipid metabolism.
31514294 0.98 SCD and FAS are the key enzymes regulating these processes, and their gene expressions are well known to increase markedly in the liver of mice fed HFD.
0.94 SCD-1, SCD-2, and FAS were significantly decreased in the HFD + 0.6% PPF group compared to the HFD control group (all p < 0.001, Figure 5), while there was no difference in the mRNA level of SREBP-1c between the two groups.
0.74 SCD inhibition rather than FAS inhibition contributed more to the anti-obesity effects of PPF.
32048816 0.98 FASN and SCD1) involved in lipogenesis were increased, and the expression of FAO enzyme Cpt1alpha was up-regulated significantly (Figure 1J-M).
0.96 FASN, SCD1 and Cpt1alpha (Figure 7D).
0.94 FASN, SCD1) involved in lipid synthesis increased.
32198362 0.98 Fasn (fatty acid synthase) and Scd1 (stearoyl-CoA desaturase) (Fig. 1c,f).
0.98 Fasn and Scd1 (Fig. 2b,c), suggesting that high concentrations of insulin and glucose can stimulate the Wnt/beta-catenin pathway in hepatocytes.
0.98 Fasn and Scd1 gene expression was significantly decreased upon treatment with the PI3K-mTORC1 inhibitors.
23219531 0.98 FAS, ACC, SCD1, mGPAT and SREBP-1c, but not CPT1, were significantly higher than those in control mice (Fig. 7A, top middle).
0.96 FAS, ACC, ACL, SCD1, mGPAT, as well as malic enzyme, G6PDH and gluconolactone dehydrogenase for NADPH synthesis (Suppl.
24069385 0.98 FASN, ACAC, ACLY, and SCD1.
0.98 FASN, and SCD1.
26074075 0.98 Fasn, Acc2, Dgat2, Ppargamma, and Cd36-were expressed at or near wild-type levels, expression of Scd1, the rate-limiting enzyme in fatty acid (FA) desaturation, increased threefold above controls (Figure 3A).
0.98 Scd1 promoter activity, without affecting the related Fasn promoter (Figure 6B).
26525535 0.98 fatty acid synthase (Fas), Scd1, 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase (Hmgcr), and HMG-CoA synthase (Hmgcs)] and enzymes responsible for the esterification of MUFA to cholesterol and TG via acyl CoA: cholesterol acyl transferase 2 (Acat2) and diacylglycerol acyl transferase 1 and 2 (Dgat1 & 2) were elevated in T5KO mice (Fig. 2A-D & F-J), including SCD1 at the protein level (Fig 2E).
0.97 Fas, Scd1, Hmgcr, Foxo1 and Lcn2 were elevated in HFD-fed T5KO mice (Fig. 3L).
26797605 0.98 FAS, stearoyl-coenzyme A desaturase1 (SCD1) and ap2.
0.97 stearyl-CoA-desaturase (SCD) and Fatty acid synthase (FAS).
26846206 0.98 fatty acid synthase (FAS), and stearoyl-CoA desaturase-1 (SCD-1).
0.98 FAS and SCD-1, leading to mitigated de novo lipogenesis in the liver in vivo.
30821074 0.98 fatty acid synthase (FAS) and stearoyl CoA desaturase 1 (SCD1), which are enzymes involved in fatty acid and triglyceride synthesis, was obviously increased in HFHS-fed mice and reduced apparently by administration of sh-YAP (Figure 4H).
0.98 FAS, ACC and SCD, are highly expressed in many cancer cells.
30921449 0.98 FAS, SCD1 and ACC.
0.97 FAS and SCD1, which participate in lipogenesis, significantly increased in the liver of the HFD-fed mice compared to the STD-fed mice (P<0.01).
31673045 0.98 fatty acid synthase (FAS), Acetyl-CoA carboxylase (ACC) and SCD1.
0.98 SCD1 deficiency, LKO mice showed lower expression of lipogenic genes namely SREBP1c, FAS, fatty acid elongase 5 (Elov5) and fatty acid elongase 6 (Elov6) compared with control mice, indicating reduced lipogenesis (Fig. 2A).
21573029 0.98 fatty acid synthase (Fasn), stearoyl-CoA desaturases-1 and -3 (Scd1 and Scd3), elongases (Elovl1, Elovl3, Elovl5 and Elovl6) and SPOT14 (Thrsp), and triglyceride synthesis enzymes including Gpam, Lpin1, Agpats (-2, -4, and -5) and Dgat1 ( Tables 8 and 9 ).
21738729 0.98 FAS, SCD1 and ELOVL6, three principal enzymes mediating de novo lipogenesis, is seen in FABP-/- mice.
22009142 0.98 SCD1), an enzyme catalyzing the synthesis of oleate, is involved in the carbohydrate-induced induction of FAS and other lipogenic enzymes.
28650445 0.98 Fasn, Scd1, Srebp1c and Chrebp in mouse livers and primary hepatocytes, supporting our current work.
30425250 0.98 SCD-1 and ACC1, were not affected by USP14 overexpression (Fig. 5c), suggesting a specific role of USP14 in FASN regulation.
29988851 0.97 FAS, and SCD-1) was decreased, and expression of genes involved in beta-oxidation (CPT-1 and PPAR-alpha) was increased due to coagonist treatment.
0.96 FAS, and SCD-1, while decreased beta-oxidation gene including CPT-1 and PPAR-alpha in kidney (Figure 3A-E).
0.96 FAS, and SCD-1, while increased renal expression of CPT-1 and PPAR-alpha in HFSTZ mice (Figure 3A-E).
0.96 FAS, and SCD-1, while increased expression of the beta-oxidation gene including CPT-1 and PPAR-alpha in these mice (Figure 3A-H).
0.96 FAS, SCD-1, CPT-1, PPAR-alpha, TNF-alpha, MMP-9 and MCP-1 in kidney.
0.94 FAS, SCD-1, CPT-1 and PPAR-alpha in kidney.
21949682 0.97 Fasn and scd-1 expressions were increased in the livers of Pgp-deficient mice and by their pivotal role in de novo fatty acids synthesis they could be major contributors of hepatosteatosis.
0.96 scd-1 was significantly increased in mdr1ab-/- mice when compared with wild-type mice (2.5-fold, p<0.01, Fig. 5A) while at 25 weeks of age, simultaneous and significant increases of fasn, scd-1 and cd36 mRNA abundance occur in mdr1ab-/- mice.
0.96 scd-1 and Fasn are overexpressed in our model and that their expressions are regulated by the nuclear receptors PPARgamma for cd36 and LXR for scd-1 and Fasn , respectively, we suggest that the turn-over of activators of these nuclear receptors, i.e., fatty acid-derived ligands or cholesterol, might be affected in Pgp deficiency.
0.93 fasn, scd-1) and xenobiotic detoxification (cyp2b10 and cyp3a11) which can be regulated either by lipids or by xenobiotics, respectively.
26679101 0.97 FAS and SCD1 in livers (Fig. 4D) but these genes were decreased in scWAT (Fig. 4E).
0.97 FAS, Elovl6 and SCD1 in liver.
0.96 FAs (SCD ratio) and FAs with 18-carbons (Elovl6 ratio) in mice.
0.58 FAS, Elovl6 and SCD1 in Fig. 4F.
23169538 0.97 stearoyl-CoA desaturase 1 as well as FAS has been reported in several established KD-fed mice models.
0.96 FAS and ACC1, and also stearoyl-CoA desaturase 1 expression.
26277244 0.97 fatty acid synthase [FASN], stearoyl-coenzyme a desaturase 1 [SCD1], and sterol regulatory element-binding protein [SREBP1]).
0.97 FASN and SCD1, the key players in de novo lipogenesis, were unregulated or down-regulated by the MD, which is different from the observation that these genes are up-regulated in the livers of mice fed high sugar diets, suggesting that the mechanism underlying the induction of hepatic steatosis by SFA is at least partially different from that of the high sugar diet.
27502578 0.97 Fasn, a rate-limiting enzyme of the lipogenic pathway, and Scd1, a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, were significantly increased (Fig. 2B).
0.96 Fasn, Scd1, Hmgcr, Cpt2, Cyp4a14, Hnf4a and Ppara) induced by BPA exposure were more significant in the older BPA mice than younger animals.
28906444 0.97 FASN and SCD1 in liver tissue were also altered.
0.95 FASN in the liver was similar between groups, expression of SCD1 mRNA was significantly higher in the livers of FFC-fed mice when compared to both control groups.
26490400 0.97 FAS, ACC and SCD, as well as LXRalpha itself.
26910791 0.97 FASN, ACAC, or stearoyl-CoA desaturase 1 (SCD1), are expressed at negligible levels in normal cells.
31554181 0.97 SCD1 inactivates AMPK phosphorylation with a consequent inhibition of its target activity as well, such as ACC, FASN and hydroxymethylglutaryl-coenzyme A reductase (a critical enzyme in cholesterol synthesis).
31573042 0.97 Fasn, DGAT1, DGAT2, ELOVL5, SREBP-1, SREBP-2, HMGCoAR, PPARgamma and SCD1, which are associated with lipid synthesis.
27499577 0.96 SCD-1, FAS, LDLR, and CYP7alpha1 in the liver.
0.96 SCD-1, FAS, LDLR and CYP7alpha1 were enhanced by HFD.
0.96 FAS and SCD-1 were increased, and PPARalpha and adiponectin were reduced in adipose tissue by HFD.
0.95 SCD-1, FAS, HMGCR, LDLR, CYP7alpha1 and PPAR-alpha proteins in the liver; and the SREBP-1, SCD-1, FAS, PPAR-alpha and adiponectin proteins in adipose tissue were reversed by PGBR.
0.95 SCD-1 (130%), FAS (320%), LDLR (31%) and CYP7alpha1 (74%) proteins, compared with the SRD group.
0.94 SCD-1, FAS and the less expressions of PPAR-alpha and adiponectin were in adipose tissue.
0.94 SCD-1 (34%), FAS (57%), HMGCR (78%), and increase in LDLR (50%), CYP7alpha1 (66%) and PPARalpha (75%) protein levels compared with the HFD group (Fig. 1).
0.94 SCD-1 (63%), FAS (48%), and increased PPAR-alpha (33%), adiponectin (33%) compared with the HFD group (Fig. 2).
0.91 SCD-1, FAS, HMGCR, increasing LDLR, CYP7alpha1 and recovering adiponectin through regulating PPARs.
0.90 SCD-1, FAS, PPARalpha, and adiponectin protein expressions in adipose tissue of high-fat diet (HFD) fed mice.
0.90 SCD-1, FAS, HMGCR, LDLR, CYP7alpha1, PPARalpha, and adiponectin in liver and adipose tissue were recovered by PGBR.
0.89 SCD-1, FAS, HMGCR, LDLR, CYP7alpha1 and PPARalpha protein expressions in liver of high-fat diet (HFD) fed mice.
0.88 FAS and SCD-1, and upregulated PPARalpha and adiponectin.
0.81 SCD-1 (217%), and FAS (71%), the lower protein expressions of the PPAR-alpha (30%) and adiponectin (53%) were found in HFD group.
0.77 SCD-1, FAS, HMGCR were decreased, and
22762794 0.96 SCD-1, FAS, PPARgamma, CD36, and LPL.
0.95 SCD-1, and FAS, and of the lipolysis-related gene, LPL.
0.75 SCD-1 by 3.6 fold and 4.0 fold (P < 0.01 for both), and that of FAS by 0.9 fold (not significant) and 0.5 fold (P < 0.05).
29922430 0.95 stearoyl-CoA desaturase-1 (SCD-1; predominantly expressed in the liver) and fatty acid synthase (FAS).
0.95 SCD-1 and FAS are key enzymes in TG synthesis and lipid homeostasis.
0.90 SCD-1 and FAS, which are enzymes related to lipid metabolism.
0.87 stearoyl-CoA desaturase-1 (SCD-1) and (B) fatty acid synthase (FAS) in the liver.
0.78 SCD-1 in the olanzapine group relative to the control group; by contrast, FAS levels in the two groups did not differ significantly.
0.61 fatty acid synthase (FAS) and stearoyl-CoA desaturase-1 (SCD-1), were measured.
29463801 0.95 SCD-1 KO mice displayed decreased FASN, LDLR and UCP-1 expression compared to wild-type.
21442273 0.94 FAS and fatty acid oxidation gene expression followed an expression pattern similar to that seen for the SCD1 null mouse indicating a potential mechanism of action for GH.
0.80 FAS mRNA was reduced; SCD1 (ste-aroyl-coenzyme A desaturase) and SCD2 mRNA did not significantly differ.
26976120 0.87 Fasn were also unchanged (Fig. 2B), suggesting that de novo fatty acid synthesis in adipose tissue of SCD1 LKO mice was not altered.
0.50 SCD1 in liver does not influence relative fatty acid synthesis gene expression including Srebf1, Acaca, Fasn and Scd1 (n = 5-8/group).
26857837 0.85 FASN, p-AKT, SCD1, LDHA/C, p-RPS6, p-4EBP1, and p-ERK1/2 (Fig. 5c and Supplementary Figure 2).



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