Publication for Scd1 and Acaca

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Scd1	stearoyl-Coenzyme A desaturase 1	20249			[link]
mmu	Acaca	acetyl-Coenzyme A carboxylase alpha	107476

Pubmed ID	Priority	Text
23762402	0.98	acc1, fas, scd1 and cd36.
	0.98	acc1, fas and scd1 (Figure 4).
	0.98	acc1, fas and scd1.
	0.98	acc1, fas and scd1.
	0.98	acc1, fas and scd1 (Figure 3), leading to elevated blood triglyceride and aggravated hepatic steatosis.
	0.98	acc1, fas and scd1 (Figures 3C to 3E), three key genes in the pathway of lipogenesis.
	0.98	acc1, fas, scd1, cd36 and pepck (Figure 4).
	0.96	acc1, fas, and scd1).
	0.88	acc1, fas and scd1, 3 vital genes involving lipogenesis, and found that the combined treatment increased their expression by 2.9+-0.5, 5.7+-0.8 and 34.8+-6.3 folds, respectively (Figures 4C, 4D and 4E).
27298813	0.98	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	SCD1 and ACC1.
	0.97	SCD1, ACC1 and FAS.
	0.95	SCD1 and ACC1.
	0.90	SCD1 and ACC1 mRNA expression as compared with silymarin at 250 mg/kg.
	0.76	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.
26608583	0.98	acetyl-CoA carboxylase 1 (ACC) and stearoyl-CoA desaturase 1 (SCD1) in mice.
	0.98	SCD1 and ACC (Fig. 3A).
	0.98	ACC and SCD1.
	0.97	SCD1 and ACC), and decreased mRNA level of genes related to fatty acid oxidation and cholesterol metabolism (Fig. 6).
	0.97	ACC and SCD1, which supported the role of SIRT1 in mediating hepatic steatosis induced by HCLD feeding.
	0.97	ACC and SCD1 induced by HCLD feeding, supported the role of those miRNAs in the pathogenesis of hepatic steatosis.
	0.86	ACC, SCD1), and down-regulated expressions of miR-122, miR-370 and miR-33; (4) decreased mRNA expressions of genes Cpt1, Pparalpha and Pgc1alpha related to fatty acid oxidation; (5) increased hepatic total cholesterol concentration and decreased expression of cholesterol metabolism related genes Abcg5, Abcg8, Abcg11, Cyp7a1 and Cyp8b1; and (6) induced higher hepatic inflammatory response accompanied with significant increased mRNA expressions of Il1beta, Tnfalpha and Mcp1.
30567368	0.98	ACC1), fatty acid synthase (FAS), and stearoyl-CoA desaturase 1 (SCD1) expression, leading to fatty liver.
	0.97	SCD1, and ACC1.
	0.97	SCD1, and ACC1, indicating that beta-conglycinin suppressed the basal expression level of these genes.
	0.97	SCD1, and ACC1 mRNA expression, indicating that the inhibition of sucrose-induced SREBP-1c activation may lead to a decrease in the liver TG content.
	0.96	SCD1, ACC1, and LPK in sucrose-supplemented mice.
	0.96	ACC1, and SCD1 was increased.
	0.92	ACC1, and LPK mRNA expression, but not in SCD1 mRNA expression compared with the high-starch-fed mice.
24067358	0.98	acetyl-CoA carboxylase1 (ACC1), fatty acid synthase (FAS) and stearoyl-CoA desaturase1 (SCD1), compared with the HF/HS-fed group (Fig. 4).
	0.98	ACC1, FAS and SCD1 in the liver.
	0.98	ACC1, FAS and SCD1 is regulated by SREBP-1c at the transcriptional level.
	0.98	ACC1, FAS and SCD1).
	0.98	ACC1, FAS and SCD1.
	0.80	ACC1, 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.
24224011	0.98	Acc) 1, and Stearoyl-CoA desaturase-1 (Scd1) were decreased by fasting in WT mice, and Keap1-KD mice exhibited an even greater decrease, suggesting enhanced Nrf2 activity promoted fasting-induced lipogenic gene reduction.
	0.98	Acc1, and Scd1 have been reported in association with reduced hepatic lipid accumulation in mouse liver.
	0.98	Acc1, and Scd1 (Figure 3), which contributed to the decreased fasting-induced hepatic steatosis and lipid accumulation.
	0.97	Acc1 and Scd1, was decreased in Keap1-KD mice by fasting than WT mice, which is in agreement with the previous observation (Figure 3B).
	0.96	Acc1 and Scd1, and reduced gene expression related to fatty acid transport in liver and WAT.
	0.95	Acc1, and Scd1, was decreased in liver of Keap1-KD (KD) mice compared to C57BL/6 (WT) mice by fasting (n=4-6 per group).
24598864	0.98	Scd1 and Acac.
	0.98	Acac and Scd1 (Table 1, Figure 6), two enzymes critical for de novo lipogenesis.
	0.97	Acac and Scd1 in hepatic tissues and cells.
	0.96	stearoyl-CoA desaturase 1 (Scd1) and acetyl-CoA carboxylase 1 (Acac1).
	0.96	stearoyl-CoA desaturase 1 (Scd1) (-2.5 fold) and acetyl-CoA carboxylase 1 (Acac1) (-1.8 fold).
25310357	0.98	Acc1 and Scd1, which are involved in hepatic fatty acid synthesis.
	0.98	Acc1, Scd1 and Cd36 in the liver, which are all associated with hepatic lipogenesis and free fatty acid transportation.
	0.98	Acc1, Fas and Scd1.
	0.95	Acc1 and Scd1, which were correlated with hepatic lipogenesis, and upregulated the gene expression of Srebf2, as previously reported.
	0.82	Acc1, Scd1 and Cd36 were significantly lower in the HF+EZ group, compared with the HF group (P<0.05; Fig. 5), while those of Srebf2 were significantly higher (P<0.01).
27333268	0.98	Acac, 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	Acaca, Acacb and Fasn levels, but a significant decrease (P<0.01) in Scd1 expression as compared with the levels found in the STD condition (Fig 3A).
	0.97	Acc-alpha/beta doublet and 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	Acaca, Acacb, and the expression of Scd1 was reduced even further (P<0.001) (Fig 3A).
	0.81	Acc-alpha/beta doublet or Fas levels, except for that of Scd1 which was reduced (P<0.001) compared with the STD group (Fig 3B).
29656110	0.98	ACC1, FAS, and SCD1), leading to markedly diminished hepatic steatosis in both study groups, with lower circulating cholesterol and triacylglyceride levels as well as reduced fat mass.
	0.98	acetyl-CoA carboxylase 1 (ACC-1), fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1), and long-chain fatty acid elongase (LCE).
	0.98	ACC1, FAS and SCD1 in DKO mice on the HFD (Figure 7C).
	0.98	ACC1, FAS and SCD1) are present in liver extracts from PS10-treated DIO mice, compared with the vehicle-treated control (Figure 7C).
	0.98	ACC1, FAS, and SCD1.
30524290	0.98	acc1, fas, scd1, c/ebpbeta, ppargamma, and srebp1) and increased the expression of genes associated with lipolysis (hsl) and lipid oxidization in white adipose tissue, in both the HFD and the EGCG groups.
	0.98	acc1, fas, scd1, c/ebpbeta, ppargamma, and srebp1) and increased the expression of genes associated with lipolysis (hsl) and lipid oxidization (pparalpha, aco2, and mcad) in epididymal adipose tissues (Figures 5, 6B).
	0.98	acc1, fas, scd1, ppargamma, and srebp1) were significantly upregulated at the mRNA level by EGCG compared with the HFD group (Figure 4), but not at the protein level (Figure 6A).
	0.97	acc1, fas, scd1, ppargamma, and srebp1) at the mRNA level but not at the protein level in subcutaneous adipose tissues (Figures 4A-E); in particular, it reduced the expression levels of srebp1 and scd1 to those observed in control mice (Figures 4C,D).
	0.94	acc1, fas, scd1, c/ebpbeta, ppargamma, and srebp1, decreased significantly in EGCG-treated mice; the protein expression level of FASN was only decreased significantly in the 100 mg/kg EGCG group, but that of ACC1 was not decreased in the HFD or EGCG groups (Figures 5A-F, 6B).
31729980	0.98	SCD1, FAS, ACC1, GPAM and DGAT2 in mouse liver.
	0.98	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).
18178930	0.98	Acc1, Scd1) but, unexpectedly, of genes involved in beta-cell differentiation, glucose sensing and electrical activity.
	0.98	Acc1 (p<0.05), Gck (p<0.05), Srebp1, Fas, Scd1 and Pdx1 gene expression was decreased in the presence of triacsin C (Figure 4).
	0.98	Acc1, Scd1) genes (Figure 2) given the previously described role of this factor in the control of lipogenic genes (20, 43) consequently for enhanced TG accumulation (Figure 1D).
	0.97	Acc1, Scd1).
24376752	0.98	acetyl-Coenzyme A carboxylase (Acaca), fatty acid synthase (Fasn), peroxisome proliferator-activated receptor gamma (Pparg), sterol regulatory element binding protein-1c (Srebf1), carnitine palmitoyltransferase 1a (Cpt1a), stearoyl-Coenzyme A desaturase 1 (Scd1), and 3-hydroxy-3-methyl-glutaryl-CoA reductase (Hmgcr).
	0.98	SCD1, glycerol-3-phosphate acyltransferase (GPAT), and ACC1 and ACC2.
	0.98	Acaca, Fasn, Scd1, Cpt1a, Ppargamma, Hmgcr, as well as the transcription factor Srebf1, leading to the suppression of de novo lipid production and eventually inhibition of hepatic steatosis.
	0.96	acetyl-Coenzyme A carboxylase (Acaca), peroxisome proliferator-activated receptor gamma (Pparg), fatty acid synthase (Fasn), stearoyl-Coenzyme A desaturase 1 (Scd1), carnitine palmitoyltransferase 1a (Cpt1a) and 3-hydroxy-3-methyl-glutaryl-CoA reductase (Hmgcr), as well as gluconeogenic genes phosphoenolpyruvate carboxykinase 1 (Pck1) and glucose-6-phosphatase (G6pc) in the liver of obese mice.
28808352	0.98	Acaca, Fasn and Scd1, and is at the same time regulated by Lxr .
	0.96	Acaca), Fatty acid synthase (Fasn), Elongation of very long chain fatty acids protein 6, (Elovl6), and Stearoyl-CoenzimeA desaturase, (Scd1) participate directly in the synthesis and elongation of fatty acids starting from Acetyl-CoA. Liver X receptor regulates the transcription of Sterol regulatory element-binding factor 1, (Srebf1), which in turn, stimulates the transcription of the enzymes mentioned above to increase the lipid biosynthesis in the liver.
	0.96	Acaca and Scd1 by androgens is supported by Kelly et al. who demonstrated that testosterone reversed the hepatic TG accumulation in androgen-deficient male mice.
	0.91	Acaca, Fasn and Scd1, and their regulators: Lxr and Srebf1c, in the liver of dams and fetuses (Fig. 6).
28808418	0.98	ACC1, stearoyl-CoA desaturase-1 (SCD1) to stimulate hepatic lipogenesis.
	0.97	SCD1, and ACC1, thereby protecting liver against high-fat or high-fat plus high-sucrose diet induced hepatic steatosis.
	0.97	SCD1 and ACC1, compared with alcohol treated control mice.
	0.97	acetyl-CoA carboxylase 1 (ACC1), stearoyl-CoA desaturase-1 (SCD1) and elongase of long chain fatty acids family 6 (ELOVL6) to synthesize FFA and TG in the liver.
29620148	0.98	ACCalpha, FAS and SCD1, induced by the HF diet, was significantly attenuated by CA (Fig. 12A).
	0.97	ACCalpha, FAS and SCD1 have been well known to play a crucial role in lipid generation.
	0.97	ACCalpha, FAS and SCD1.
	0.77	ACCalpha, FAS and SCD1 were also elevated in the mice fed the HF diet.
30274245	0.98	Acc1, Scd1, and Elovl6, and adipocyte differentiation such as Pparg2, Cebpa, and Fabp4.
	0.98	ACC1), fatty acid synthase (FASN), stearoyl-CoA desaturase-1 (SCD1), and ChREBP-beta.
	0.97	ACC1, and stearoyl-CoA desaturase-1 (SCD1).
	0.97	Acc1, and Scd1 were up-regulated in BAT.
31083413	0.98	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).
	0.97	Acc1, Scd1, Scd2, Gpam, Dgat1, and Dgat2, inhibiting hepatic fatty acid and TG synthesis.
	0.97	Acc1, Scd1, Scd2, Gpam, Dgat1, and Dgat2.
	0.95	acetyl-CoA carboxylase 1 (Acc1), stearoyl-CoA desaturase-1 (Scd1), Scd2, glycerol-3-phosphate acyltransferase (Gpam), diacylglycerol O-acyltransferase 1 (Dgat1), and Dgat2.
31484323	0.98	steraroyl coenzyme decarboxylase 1 (Scd1), peroxisome proliferator-activated receptor gamma (PPARgamma), acetyl-CoA carboxylase 1 (Acaca), and glycerol-3-phosphate acyltransferase, mitochondrial (Gpam), which were mitigated by IAA treatment.
	0.98	steraroyl coenzyme decarboxylase 1 (Scd1), peroxisome proliferator-activated receptor gamma (PPARgamma), fatty acid synthase (Fasn), acetyl-CoA carboxylase 1 (Acaca), diacylglycerol O-acyltransferase 2 (Dgat2), and glycerol-3-phosphate acyltransferase, mitochondrial (Gpam), which were related to lipogenesis (p < 0.05) (Figure 4A).
	0.98	Scd1, PPARgamma, Acaca, and Gpam was abated by IAA treatment, thereby bringing about a reduction in hepatic triglyceride accumulation.
	0.96	Scd1, PPARgamma, Acaca, and Gpam (p < 0.05).
20953342	0.98	Acaca, Gpd1, Agpat2, 6, Scd1) and are likely associated to the RSG-mediated increase in hepatic trioleate levels.
	0.98	Acaca, Fas, Scd-1, or Agpat.
	0.94	Acaca, +87%, P < .001), the fatty acid synthase (FAS, +270%, P < .001), and the stearoyl-Coenzyme A desaturase (Scd1, +455%, P < .001) or was involved in the pentose phosphate pathway such as the transketolase (Tkt, +74%, P < .001) and phosphogluconate dehydrogenase (Pgd, +117%, P < .001).
22988513	0.98	Acaca (CLA = 0.72 versus control = 0.22) and Scd (CLA = 0.05 versus control = -0.92) expression was upregulated in response to trans-10, cis-12-CLA.
	0.97	Acaca, Gpam, Scd, Pck1, Plin2).
	0.96	Acaca, Scd, and Gpam in mice fed trans-10, cis-12-CLA suggested that the liver was generating more palmitic acid and oleic acid (see Table 3) and esterifying it into TG.
24982757	0.98	ACACA, FASN, SCD1, and A-FABP) were significantly higher in cells overexpressing DGAT2 than in control cells.
	0.97	acetyl CoA carboxylase (ACACA), FA synthase (FASN), stearoyl-CoA desaturase-1 (SCD1), and FA-binding protein (a-FABP) was significantly higher in 3T3-L1 adipocytes overexpressing DGAT2 than in control cells.
	0.97	ACACA, FASN, A-FABP, and SCD1 was significantly higher in 3T3-L1 adipocytes overexpressing DGAT2 than in control cells, as was the mRNA expression of FAT/CD36 and PPARgamma.
26237535	0.98	Scd1, Acaca, and Fasn mRNA.
	0.96	Scd1, Acaca, and Fasn mRNA in both genotypes (Figs. 3B, 3C, 3D).
	0.95	Scd1 (Fig. 2A), Fasn (Fig. 2B), Acaca (Fig. 2C), Ucp1 (Fig. 2D), Ppargc1a (Fig. 2F), and Adrb3 (Fig. 2G) in IWAT of WT mice, but in each instance MR failed to change mRNA levels for any of these genes in ob/ob mice.
26476289	0.98	acetyl-CoA carboxylase (ACAC), fatty acid synthase (FASN), and stearoyl-CoA desaturase 1 (SCD1).
	0.97	ACAC, ACLY, SCD1, nuclear/activated sterol regulatory element-binding protein 1 (SREBP1), and pyruvate kinase M2 isoform (PKM2) were highest in AKT mice, whereas lactate dehydrogenase A/C (LDHA/C) displayed equivalent protein levels in AKT and AKT/Cre livers (Fig. 4, 5, Supplementary Fig. 5).
	0.97	ACAC, SCD1, nuclear (n)SREBP1, LDHA/C, PKM2) were downregulated in AKT/Cre mice when compared with AKT mice.
29057818	0.98	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	SCD1 and ACC1 in hepatocytes.
	0.97	SCD1 and ACC1, while decreasing the expression of HSL in the intramuscular fat tissue.
29884546	0.98	acetyl CoA carboxylase 1 (Acc1), fatty acid synthase (Fas) and stearoyl CoA desaturase 1 (Scd1), were upregulated in Tlr4fl/fl mice after chronic alcohol consumption relative to pair-fed mice (Figure 1D).
	0.98	Acc1, Fas, and Scd1.
	0.97	ACC1, FAS, and SCD1 tended to be reduced in Tlr4LKO mice after chronic alcohol intake (Supplemental Figs. 1a and b).
29890650	0.98	ACC1 and FASN are two key enzymes involved in lipogenesis, helping acetyl-CoA to form palmitic acid desaturated by SCD1.
	0.97	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	ACC1 (acetyl-CoA carboxylase-1), 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.
30081561	0.98	ACC1, FAS and SCD1.
	0.97	ACC1), fatty acid synthase (FAS), and stearoyl-CoA desaturase-1 (SCD1) were significantly decreased after Tm administration.
	0.97	ACC1, FAS and SCD1 promoted hepatic lipid accumulation and induced liver steatosis.
30463189	0.98	SCD-1, ACC1, and PCK1-alpha) in liver tissues of HFD-fed mice (p < 0.01) (Figure 6C).
	0.96	SCD-1 is a microsomal enzyme required for the synthesis of oleate and palmitoleate, and ACC-1 is a major enzyme in de novo fatty acid biosynthetic pathway.
	0.94	SCD-1, and ACC-1.
31123488	0.98	ACC1, and SCD1.
	0.96	ACC1, SCD1) expression and enzyme activity (ME).
	0.95	ACC1, SCD1, and PPARgamma were significantly decreased by PY supplementation, ME activity was decreased compared to that in the HFD group, and hepatic lipid droplet size and number were reduced, presumably owing to its anti-lipogenic effects.
31952262	0.98	SCD-1, ACC1.
	0.97	ACC1, and SCD-1 protein levels in the liver.
	0.96	SCD-1, ACC1, and HMGCR.
18840360	0.98	SCD1, and ACC1 were decreased in livers of HFD-fed DT-treated CD11c-DTR BMT mice while PPARalpha expression was unaffected.
	0.96	stearoyl CoA desaturase-1 (SCD1) and acetyl-CoA carboxylase 1 (ACC1), and peroxisome proliferator-activated receptor (PPAR) alpha, a key regulator of hepatic lipid oxidation.
22936178	0.98	SCD-1, ACC-1, ACC-2, and CD36 (Fig. 4B).
	0.97	SCD-1, ACC-1, and PPARgamma expression and activated p-ACC at the protein level.
23738334	0.98	Acaca, Fasn, and Scd1 as well as Atgl were upregulated in iWAT from mice fed C7F compared to the three other groups (Figure 5(B)).
	0.73	Acaca (acyl-CoA carboxylase 1), Fasn (fatty acid synthase), and Scd1 (stearoyl-CoA desaturase 1)) and synthesis of triglycerides (Gpam (glycerol phosphate acyltransferase) and Dgat2 (diglyceride acyltransferase 2)).
23919961	0.98	Acc1, and Scd1 were increased in parallel with Srebp1c (Fig. 5D).
	0.98	Scd1, Fas, and Acc1 (Fig. 5F).
24339864	0.98	Acaca, Acly, Elovl, Scd1) and the transcription factors that regulate their expression (Lxr-alpha, Srebp1, Chreb, and Nr1h3) in WAT.
	0.98	Acaca, Acly, Fasn, , Elov16, and Scd1) were affected by loss of Sfrp1.
28400497	0.98	Acaca, Scl25a1, Scd1, and Fasn, reflected the development of an increased capacity for fat accumulation (Fig. 3A and C).
	0.98	Acaca, Scl25a1, Scd1, and ChREBP in the inguinal fat.
28732092	0.98	Acaca, Acacb, Fasn, Elovl6 and Scd1 in an LXR dependent manner (Fig 3A).
	0.96	Acaca, Fasn, Scd1, Srebp-1c and Chrebp promoters.
30772256	0.98	acetyl-CoA carboxylase 1 (Acc1) and stearoyl-CoA desaturase 1 (Scd1) in both genotypes (Figure 4B and C), suggesting that hepatic lipogenesis was reduced.
	0.96	Acc1 and Scd1 mRNAs.
31546946	0.98	Acaca expression by forming a tetrameric complex with TR/RXR, which is important to note because Acaca is an earlier target of Srebf1 in the lipogenesis process, followed by Fasn, Scd1, and other lipogenic genes.
	0.94	Acaca, and Fasn), fatty acid esterification (Dgat2), fatty acid beta-oxidation (Sirt1, Ppargc1, and Acox1), and fatty acid desaturation/elongation (Scd1, and Elovl6) were in good agreement with current transcriptomics results (Figure 7A,B).
24039619	0.98	SCD1 activity leads to accumulation of saturated fatty acids, which inhibit acetyl-CoA carboxylase 1 (ACC1), and subsequently decreases de novo synthesis.
26846206	0.98	acetyl-CoA carboxylase-1 (ACC1), fatty acid synthase (FAS), and stearoyl-CoA desaturase-1 (SCD-1).
26905426	0.98	ACC1), stearyl-coA desaturase-1 (SCD1), glycerol phosphate acyltransferase-1 (GPAT), and peroxisome proliferator-activated receptor gamma (PPARgamma) (Fig. 5D), compared with their abundance in animals fed HFrD alone.
27480224	0.98	ACC-1, induced expression of lipogenic genes, such as FASN, SREBP-1c, and SCD-1 (Fig. S14B) and increased cellular FFA and TG levels (Fig. S14C).
28650445	0.98	Acaca, Fasn, Scd1, Srebp1c and Chrebp in mouse livers and primary hepatocytes, supporting our current work.
24946098	0.97	SCD1 (2.9-fold) and ACC1 (2.4-fold) mRNA levels in WT mice compared to vehicle treated controls (Figure 6A-D).
	0.93	SCD1 and ACC1 mRNA remained unchanged (Figure 6A-D).
	0.88	stearoyl-Coenzyme A desaturase 1 (SCD1), acetyl-CoA carboxylase 1 (ACC1) and acetyl-CoA carboxylase 2 (ACC2).
26035386	0.97	Acaca (P<0.05), Acacb (P<0.001), Fasn (P<0.001) and even Scd1 (P<0.001).
	0.97	Acaca, Acacb, Fasn and Scd1 genes was upregulated after 6 h of the cytokine exposure .
	0.96	ACCalpha and ACCbeta), fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD1).
26120082	0.97	SCD1), and acetyl-CoA carboxylase-1 (ACC1) acting downstream of glycolysis.
	0.97	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	ACC1, SCD1, and SREBP1c activity have been shown to reduce proliferation and induce apoptosis in cancer cells.
28356106	0.97	SCD-1, FAS, and ACC-1 were observed in the DHA/EPA 1:2 group, which indicated that supplementation with DHA/EPA is likely to alter fatty acid synthesis via upregulating AMPK expression, which decreases the expression of SREBP-1C and PPARgamma, thereby reducing downstream expression of key enzymes (ACC-1, FAS, and SCD-1) in the liver.
	0.91	SCD-1 (stearoyl-CoA desaturase-1), FAS (fatty acid synthase), ACC-1 (acetyl CoA carboxylase-1), and PPARgamma (peroxisome proliferator activated receptor gamma) mRNA expression, while the DHA/EPA 1:1 group showed higher HSL (hormone sensitive lipase), PPARalpha, and CPT-1 (carnitine palmitoyl transferase-1) mRNA expression, among the DHA/EPA groups.
	0.76	SCD-1, FAS, ACC-1, and HSL, which are proteins involved in lipogenesis; and AMPK, PPARalpha, PPARgamma, CPT-1, and ACOX, which are proteins involved in fatty acid oxidation.
21178610	0.97	ACC1, 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	ACC1 and ACC2), 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.
23349485	0.97	ACC1, SCD1, PPARgamma, and DGAT2, observed in HFD-fed Crbn KO mice suggests that inhibition of hepatic lipogenesis may contribute to lower levels of fat accumulation.
	0.93	ACC1 and SCD1 mRNA were significantly lower in HFD-fed Crbn KO mice than in HFD-fed WT (Fig. 7F and G).
23507082	0.97	acetyl CoA carboxylase 1 (Acc1) and Steroyl CoA desaturase 1 (Scd1) protein expression.
	0.97	acetyl CoA carboxylase 1 (pAcc1), Acc1, and Scd1 protein levels were increased in Keap1-KD mice fed HFD compared to C57BL/6 mice.
28327662	0.97	Acc1, Acc2), glycerol-3-phosphate acyltransferase (Gpat) family members, 1-acylglycerol-3-phosphate-O-acyltransferase (Agapt) family members and diacylglycerol acetyltransferase 2 (Dgat2) were not significantly changed at mRNA levels in the mutants (Supplementary Table 2; Supplementary Fig. 4), the mRNA levels of Fasn, Elovl6, and Scd1 were decreased by 42-74% in chow or HCD-fed LZB20KO liver relative to control (Fig. 3b).
	0.96	Acc1 and Gpat are the important ChREBP targets for lipogenesis, their expression was not significantly changed by the loss of Zbtb20, probably because of their relatively weaker responsiveness to the decrease of ChREBP dosage than other targets (for example, Elovl6, Scd1) and the compensatory effects of other transcription factors (for example, SREBP1c).
28420650	0.97	stearoyl-CoA desaturase 1 (SCD1), and acetyl-CoA carboxylase 1 (ACC1).
	0.96	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).
31579588	0.97	ACC1 or SCD1, are controlled by the transcription factor FoxO1.
	0.96	ACC1 and SCD1 are two other key enzymes involved in lipogenesis (29925265).
24438079	0.97	acetyl-CoA carboxylase (ACC; Acaca) but not stearoyl-CoA desaturase 1 (SCD1; Scd1) were elevated in HFSC- compared to HFC-fed LDLR-/- mice after 16 weeks of treatment (Figure 5A-C).
27058520	0.97	SCD1, and ACCalpha are involved in the biosynthesis of fatty acids while ACOX and CPT1alpha are related to fatty acid oxidation.
30504766	0.97	Scd genes, Acss2 (Acyl-coenzyme A synthetase short-chain family member 2, listed in Fig. 3b), but not that of Acly (ATP citrate lyase), Acaca (acetyl CoA carboxylase 1), or Elovl6 (ELOVL family member 6, elongation of long-chain fatty acids) in the adipose tissue of HFD-fed mice or age-matched chow-fed mice (Fig. 4a).
31668396	0.97	acetyl-CoA carboxylase 1 (Acc1) (1.8-fold lower, P < 0.05) and fatty acid synthase (Fas) (3.1-fold lower, P < 0.01) and nearly complete suppression of stearoyl CoA desaturase 1 (Scd1) (36-fold lower, P < 0.001) expression as compared to WT mice on HFD.
29389988	0.96	stearoyl-Coenzyme A desaturase 1 (SCD-1), acetyl-CoA carboxylase alpha (ACCalpha) and fatty acid elongase 6 (Elovl6) compared to the control, cis-9,trans-11 CLA and LA conditions.
	0.82	ACCalpha (r = 0.510, p = 0.03), but not with SREBP-1c (r = 0.415, p = 0.09), SCD-1 (r = 0.457, p = 0.06) and hepatic lipid content (r = 0.215, p = 0.39).
30692584	0.96	Acaca and Scd1 was less in the DNT5 group when using the linear random effects model and the Mann-Whitney test, respectively, consistent with down-regulated Srebp1c gene expression (Fig. 6C).
	0.84	acetyl-CoA carboxylase 1 (Acaca) and the fatty acid synthase (Fasn) and the stearoyl-CoA desaturase 1 (Scd1).
23169538	0.96	ACC1, and also stearoyl-CoA desaturase 1 expression.
24098955	0.96	Acaca, Figure 4g), but the 9 desaturase (Scd1) was significantly lower in FPH treated mice (Figure 4h).
23672804	0.95	ACACA, ASCL5 and SCD1 are important lipogenic genes.
	0.91	ACACA, ACSL5, FABP5, HMGCR, SCD1, and scavenger receptors.
27801862	0.95	SCD-1 and D6D activities and ACC1 expression and DNL were reported in the liver from the HCD group.
30642871	0.95	Acaca and Dgat2 and increasing Scd-1 expression.
31149661	0.94	Acaca, Fasn and GPAT decreased significantly, while Scd1 increased 3.28-fold in EYHDL than in HFD, leading to less contents of SFA in EYHDL and further neutralizing the upregulation effect of the HFD (p<0.05).
	0.91	Acaca, Fasn, GPAT and Scd1.
32047441	0.93	SCD1, ACC1, and ACOX1) were unaffected after PEA administration.
	0.89	SCD1, ACC1, and ACC2), fatty acid oxidation-related genes (CPT-1alpha and ACOX1), and the triglyceride hydrolysis-related gene LPL in LG tissue were measured using RT-PCR ( Figure 4 ).
29159325	0.93	ACC1, ACC2, FAS, and SCD1.
30669332	0.93	Acetyl-CoA carboxylase-1 (Acc1, -38%, p < 0.05), Stearoyl-CoA desaturase-1 (Scd-1, -42%, p < 0.01), Sterol regulatory element-binding protein-1 (Srebp-1, -25%, p = 0.06), and Diacylglycerol O-acyltransferase-1 (Dgat-1, -21%, p < 0.05) as lipogenic genes.
26856717	0.92	ACC1, FAS and SCD1 than HFD.
27904876	0.91	acetyl CoA carboxylase-1 (ACC1) and stearoyl CoA desaturase-1 (SCD1).
31558861	0.90	stearoyl coenzyme A desaturase 1 (SCD1), fatty acid synthase (FAS) and acetyl-CoA carboxylase 1 (ACC1), were determined.
26976120	0.85	Acaca and Fasn were also unchanged (Fig. 2B), suggesting that de novo fatty acid synthesis in adipose tissue of SCD1 LKO mice was not altered.
25797050	0.72	acetyl-CoA carboxylase 1 (ACC1) (a) and stearoyl-CoA desaturase 1 (SCD1) (b) in fully differentiated 3T3-L1 adipocytes.
31667363	0.52	ACC1/2, FAS, and SCD1, was not altered (Fig. 5b).