Publication for Fasn and Hmgcr

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Fasn	fatty acid synthase	14104			[link]
mmu	Hmgcr	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	15357

Pubmed ID	Priority	Text
27502578	0.98	Fasn and Hmgcr (Fig. 6A-D).
	0.98	Fasn and Hmgcr were hypomethylated in the BPA-exposed mice, which is very likely to contribute to the promoted transcription of Srebf1 and Srebf2 and their targets.
	0.97	Fasn and Hmgcr (Fig. 5A-D).
	0.97	Fasn, Srebf2 and Hmgcr (Fig. 7A-D).
	0.97	Fasn, and, knockdown of Srebf2 decreased Hmgcr expression (Fig. 7E-H).
	0.97	Fasn and Hmgcr, respectively.
	0.97	Fasn expression by Srebf1 knockdown and downregulation of Hmgcr expression by Srebf2 knockdown were compromised by BPA treatment.
	0.96	Fasn, CpG sites 2, 5 of CGI-A of Hmgcr and CpG sites 1, 2, 7 of CGI-B of Hmgcr (Fig. 5A-D).
	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.
	0.96	Fasn, and, Srebf2 with Hmgcr.
	0.96	Fasn and Hmgcr induced by BPA treatment also progressed with treatment duration.
	0.93	Fasn is the key enzyme of fatty acid and Hmgcr is the key enzyme of cholesterol synthesis.
	0.93	Fasn and Hmgcr decreased with aging in our BPA and control mice.
	0.91	Fasn, CpG sites 1, 2, 5 of CGI-A of Hmgcr and CpG sites 1, 7, 11 of CGI-B of Hmgcr.
	0.89	Fasn and Hmgcr also decreased with aging in both groups.
	0.88	Fasn and Hmgcr in the BPA-exposed mice were significantly lower than the control mice.
	0.87	Fasn, CpG sites 1of CGI-A of Hmgcr and CpG sites 1, 7 of CGI-B of Hmgcr.
	0.77	Fasn expression by Srebf1 knockdown and downregulation of Hmgcr expression by Srebf2 knockdown were compromised by BPA treatment compared with the control (treated with DMSO).
	0.60	Fasn and Hmgcr, which are the downstream targets of Srebf1 and Srebf2, respectively.
30821074	0.98	fatty acid synthase (FAS) and 30-hydroxylmethyl glutaryl coenzyme A reductase (HMGCR), thereby stimulating their transcription and promoting hepatocyte lipogenesis and cholesterol synthesis.
	0.98	FAS and HMGCR, are essential for their transcriptional regulation in response to insulin.2 ChIP experiments revealed that YAP was present at the SREBP-binding motifs at the promoter regions of both FAS and HMGCR (Figure 6A).
	0.98	FAS and HMGCR, showing that YAP could bind to the SREBPs and form a complex at their promoters (Figure 6B,C).
	0.98	FAS and HMGCR (Figure 7A,B).
	0.98	FAS and HMGCR through nuclear translocation of SREBPs, Lats1 overexpression reversed these effects (Figure 7D,E).
	0.97	FAS and HMGCR (Figure 6F,G).
	0.95	FAS and HMGCR exposed to HG plus insulin were inhibited by sh-YAP treatment in primary hepatocytes.
	0.94	FAS and HMGCR in liver, key enzymes for the synthesis of triglyceride and cholesterol, were also reduced by Lats1 overexpression (Figure 2E).Consistently, haematoxylin and eosin (H&E) staining and oil red O staining experiments indicated administration of ad-Lats1 reduced excess fat accumulation in hepatic intracellular vacuoles (Figure 2G).
	0.94	FAS and HMGCR exposed to HG plus insulin were inhibited by ad-Lats treatment in primary hepatocytes.
	0.91	FAS and HMGCR promoters.
	0.86	FAS and HMGCR mRNA and protein levels.
	0.51	FAS and HMGCR, luciferase vectors of FAS (FAS-luc) and HMGCR (HMGCR-luc), containing one SREBP DNA-binding site, were generated.
30954949	0.98	Hmgcr, Sqle, Mvd and Elovl6 were homogeneously upregulated, whereas Fasn expression was strongly downregulated, in Fasn(-) HCCs (online supplementary figure S8).
	0.98	Hmgcr, Sqle and Mvd (figure 2D), resulting in highest CE levels in Fasn(-) HCC (figures 2D and 4D).
	0.98	Fasn promotes nuclear localisation and activation of sterol regulatory element binding protein 2 (Srebp2), which upregulates the key enzyme Hmgcr of cholesterol biosynthesis, resulting in cholesterol accumulation and, eventually, HCC formation.
	0.98	FASN and HMGCR is likely to prevent triglyceride and cholesterol accumulation, leading to strong suppression of hepatocarcinogenesis.
	0.97	FASN resulted in nuclear localisation of SREBP2 (figure 6C, D), as well as increased HMGCR mRNA expression (figure 6E).
	0.94	Hmgcr, squalene monooxygenase (Sqle) (padj=0.057), diphosphomevalonate decarboxylase (Mvd), which are involved in the mevalonate and cholesterol biosynthesis pathways, were highest in Fasn(-) HCCs and cytochrome P450 family 7 subfamily a member 1 (Cyp7a1) (padj=0.205) and cytochrome P450 family 7 subfamily b member 1 (Cyp7b1), two key enzymes responsible for cholesterol ester (CE) degradation, were lowest in the same tumours (figure 2B and D).
	0.78	Hmgcr, Mvd and Sqle in Fasn(+) and Fasn(-) HCCs from PIK3CA/c-Met and PIK3CA/Ras mice.
	0.77	FASN and HMGCR may be required for the effective prevention or treatment HCC (figure 8).
25402228	0.98	Fasn and Srebf1 and cholesterologenic Hmgcr and Hmgccs1 genes point to, but do not prove, increased de novo lipogenic and cholesterologenic states in the liver consequent to augmented intestinal ME1 expression.
	0.97	Fatty Acid Synthase (FASN) and HMG-CoA Reductase (HMGCR), respectively.
	0.97	Fatty Acid Synthase (Fasn), Stearoyl CoA Desaturase 1 (Scd1), Retinoid X Receptor Gamma (Rxrg), Lipoprotein lipase (Lpl), HMG-CoA Reductase (Hmgcr), 3-hydroxy-3-methylglutaryl-CoA Synthase 1 (Hmgcs1), and Gardner-Rasheed Feline Sarcoma viral (Fgr) oncogene homolog were all up-regulated in jejunums of ME1-Tg mice.
	0.97	Fasn, Srebf1, Hmgcr, Hmgcs1, Prkce and Ldlr (Ldl Receptor), decreased Apoe expression, and unchanged expression of Apoa1 and Cyp4a10 in livers of ME1-Tg compared to WT controls (Figure 5A, H).
	0.96	Fasn, Srebf1, Pparg, Hmgcr, Hmgcs1, Ldlr, Apoa1, Apoe and Cyp4a10 genes, while Prkce transcript levels were decreased in livers of ME1-Tg compared to WT controls (Figure S2A-B).
27385127	0.98	FASN), acetyl-CoA carboxylase (ACC) and HMGCR were dramatically reduced when SREBP maturation was prevented, and this effect correlated with decreased intracellular cholesterol synthesis.
	0.98	FASN, ACC and HMGCR are main targets.
	0.98	FASN and ACC) and the cholesterol (HMGCR) pathways.
	0.97	FASN and the SREBP-2 target gene HMGCR was significantly decreased following S1P inhibition at 1, 2 and 3 days after inhibitor treatment, compared with controls.
	0.94	HMGCR mRNA expression was observed which was associated with a more modest reduction at the protein level than what was detected for FASN and ACC.
29316698	0.98	FASN and HMGCR are found in keratinocyte and are involved in the synthesis of fatty acid and cholesterol, which are components of keratinocyte-derived lipids.
	0.98	FASN and HMGCR, which are lipid synthesis enzymes in keratinocytes, are upregulated in irradiated skin in the latent stage.
	0.97	fatty acid synthase (FASN) and 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR) in keratinocytes, and play a role in the maintenance of the epidermal barrier.
	0.96	FASN and HMGCR could be a comprehensive effect that improves skin permeability in irradiated skin.
	0.95	FASN and HMGCR expressions in irradiated skin could be a comprehensive effect for skin barrier recovery.
23080229	0.98	HMG-CoAR, FAS and CYP7A1.
	0.97	FAS, HMG-CoAR and C/EBP-beta was blunted in CHOP-/- mouse primary hepatocytes.
	0.97	FAS, HMG-CoAR and C/EBP-beta was inhibited in CHOP-/- mice.
	0.97	HMG-CoAR, FAS, and C/EBPbeta, and reduced CYP7A1 expression.
25083875	0.98	fatty acid synthase (Fasn), 3-hydroxy-3-methyl-glutaryl-CoA reductase (Hmgcr), and lanosterol synthase (Lss) were uniquely regulated by SIRT6, as the amplitude of circadian oscillation was enhanced in SIRT6 KO (Figure 2E).
	0.98	Fasn, Hmgcr, and Lss (Figure 2D).
	0.86	Fasn, Hmgcr, and Lss genes with increased circadian amplitude exclusively in SIRT6 KO versus WT.
	0.70	Fasn promoter illustrating selective SREBP-1 recruitment to the TSS versus negative control regions, as well as recruitment to the Hmgcr and Lss promoters, is shown (Figures 5C and S8).
28701865	0.98	fatty acid synthase (FAS), and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA), as expected.
	0.97	fatty acid synthase, and 3-hydroxy-3-methylglutaryl coenzyme A reductase, were increased, whereas that of the lipolytic enzyme carnitine palmitoyltransferase-1 was decreased.
	0.97	FAS, and HMG-CoA, and lipogenic factor aP2 were downregulated by 83.5%, 73.9%, 94.5%, 33.1%, and 99.4%, respectively, in SG-treated adipocytes compared with cells stimulated with MDI alone.
	0.82	FAS, FATP1, and HMG-CoA by RT-PCR analysis.
28867797	0.98	FAS, ACC and HMGCR.
	0.97	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and fatty acid synthase (FAS) were markedly up-regulated in the livers of HFD group as compared with the control group.
	0.94	HMGCR, SREBP-1c and FAS expressions and the increase in CPT1 and phosphor-IRS-1 expressions.
29997677	0.98	fatty acid synthase (FAS), and HMG-CoA reductase (HMGR) were downregulated by KPE in a dose-related manner (Figure 3(c)).
	0.98	HMGR, FAS, and LPL (Figure 3(c)).
	0.97	HMGR, and FAS.
30619997	0.98	HMGCR KI cells may have been provided by elevated expression of lipogenic genes because the mRNA expression of key enzymes in lipid synthesis, such as ACC-alpha (Acaca), ACC-beta (Acacb), and fatty acid synthase (Fasn), was significantly up-regulated without significant changes (albeit a trend) in the expression of the upstream transcriptional regulator Srebf1 (Fig. 6B,C).
	0.98	HMGCR KI mice, the increase in hepatic triglyceride is accompanied by increased glucose output from the liver as well as increased mRNA expression of the SREBP1c gene targets Fasn, Acaca, and Acacb.
	0.60	Fasn, Acaca, and Acacb, from livers of high-carbohydrate-fed WT and HMGCR KI mice.
18677445	0.98	HMGCR, FASN, SREBP2, S1P, and SQS1).
	0.94	HMGCR, DHCR7, FASN, SREBP2, SCAP, S1P, and SQS1) showed significantly reduced expression in NRIF-shRNA-transfected cultures compared to cells transfected with non-silencing shRNA, regardless if the cells were grown in regular or cholesterol-deficient cell culture media
24430730	0.98	fatty acid synthase (Fas) in the FA synthesis pathway, and 3-hydroxy-3-methylglutaryl-CoA reductase (hmgcr) in cholesterol synthesis.
	0.82	Fas, Srebpf-1c], fatty acid oxidation [pparalpha, acyl-coenzyme A thioesterase (Acot1)], lipoprotein [lipoprotein lipase (Lpl)] and cholesterol metabolism [hmgcr] (Fig. 3b and Supplementary Fig. S2), and found several of these rhythmic genes had changes in their temporal profiles: ACC was elevated at almost all time points (ZT0-ZT12, ZT20); Acot1 was elevated at ZT4; while Fas had an additional late peak at ZT16 and ZT20.
24608444	0.98	fatty acid synthase (FAS) and HMG-CoA reductase (HMGCR), SREBPs promote the biosynthesis of fatty acids, triglycerides, and cholesterol.
	0.97	FAS, HMGCR, HMGCS, and LDLR, were expressed at significantly lower levels in response to BF175 treatment.
25072708	0.98	FAS, and HMG-CoA reductase.
	0.97	FAS (3E), and SREBP-2, HMGCR, and LDLR mRNA levels (3F) in concentration dependent manner.
27840945	0.98	FAS, SCD1 and HMGCR), which demonstrated a significant reduction in both the mRNA and protein levels.
	0.94	FAS and HMGCR, the two essential lipogenic enzymes, was further confirmed by immunohistochemical analysis of the hepatic sections (Fig. 3B).
27929393	0.98	FAS, SREBP-1C, SREBP-2, and HMGCR.
	0.96	fatty acid synthase (FAS), peroxisome proliferator activated receptor gamma (PPARgamma), sterol regulatory element-binding protein-1C (SREBP-1C), sterol regulatory element-binding protein-2 (SREBP-2), acetyl-CoA carboxylase (ACC), HMG-CoA reductase (HMGCR), ATP-binding cassette transporter G5/G8 (ABCG5/8), cholesterol 7 alpha-hydroxylase (CYP7A1), and sterol 12-alpha-hydroxylase (CYP8B1), as well as oxidative stress markers, including superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), glutathione peroxidase (GPX), and catalase, were also regulated by XB supplementation.
31270932	0.98	FAS, SREBP2 and HMGCR, and up-regulated glycogen synthesis proteins, including Akt2 (Ser474) phosphorylation, GLUT2 and GSK-3beta, in the liver of obese mice.
	0.97	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.
25038053	0.98	FAS, ACC, HMGCR, and LDLR.
27582413	0.98	fasn, acc and scd-1, as well as hmgcs, hmgcr and ldl-receptor (Fig. 2B and Supplementary Fig. S2B).
27707816	0.98	HMG-CoA reductase (Hmgcr), as well as the SREBP-1c target gene, Fasn, indicating SCAP loss of function (supplemental Fig. S1C, D).
29183708	0.98	HMGCR, acetyl-CoA carboxylase (ACC) and fatty-acid synthase (FASN), resulting in reduced cancer cell proliferation, invasion and migration.
31604978	0.98	3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), decreases fatty acid synthase (FAS) expression, and activates malonyl-CoA carboxylase, which leads to a reduction in fatty acid and cholesterol synthesis.
32111832	0.98	HMGCR, LDLR, SQLE, and FASN in response to sterol-depletion, in Hap1-SPRINGKO cells basal expression of these genes was reduced and the response to sterol-depletion was largely abrogated.
23702383	0.97	FAS, SREBP 1c and HMGR abundance, and increased the ratio of ACC p/ACC without affecting CPT-1 (Fig. 6), PPAR alpha and PGC-1alpha in comparison with HFD animals, suggesting that SCO reduces triglyceride and cholesterol accumulation in the liver by suppressing de novo lipogenesis instead of altering fatty acid oxidation.
	0.94	FAS, HMGR, and SREBP protein abundance in the liver without altering CPT 1 in compared with HFD mice, but SANT only significantly reduced FAS content.
	0.85	FAS, SERBP 1c, and HMGR content, and increased ratio of ACC p/ACC, but did not affect CPT-1 abundance in the liver in comparison with HFD group.
	0.83	fatty acid synthase (FAS), HMG-CoA Reductase (HMGR), and Sterol regulatory element-binding protein 1c (SREBP1c), but not Carnitine palmitoyltransferase I (CPT-1) when compared with HFD group.
19556020	0.97	fatty acid synthase (FAS) and acetyl coenzyme-A carboxylase (ACC), whereas SREBP-2 activity has been more closely linked to regulation of genes involved in cholesterol synthesis and uptake, such as low-density lipoprotein receptor (LDLR) and 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR).
	0.96	FAS and ACC were detected, whereas those of LDLR and HMGCR were not, suggesting the activation of SREBP-1 but not SREBP-2 (Fig. 4A).
	0.72	FAS and ACC for SREBP-1 and LDLR and HMGCR for SREBP-2.
31573042	0.97	Fasn, DGAT1, DGAT2, ELOVL5, SREBP-1, SREBP-2, HMGCoAR, PPARgamma and SCD1, which are associated with lipid synthesis.
	0.92	Fasn, SREBP-1 and HMGCoAR were decreased in the HFD groups and in the NFD groups treated with low or high-doses of DADS compared with the NFD control group.
	0.57	Fasn, SREBP-1 and HMGCoAR were decreased in the HFD groups and in the NFD groups treated with low and high-doses of DADS compared with the NFD control (for Fasn, NFD-AL and HFD-AH vs. NFD-CON, P<0.01; NFD-AH, HFD-CON and HFD-AL vs. NFD-CON, P<0.05.
31749969	0.97	FASN, ELOVL6 and ACCalpha were significantly lower in IL-1alpha KO compared with Loxp mice (figure 6A), with similar levels of DGAT, LXR, Srebpf-1c, ChREBP, HMGCR, Cyp7a and LDLR (Fig. 6A and online supplementary fig. S1).
	0.83	fatty acid synthase (FASN), elongation of long-chain fatty acids family member 6 (ELOVL6), acetyl-CoA carboxylase alpha (ACCalpha), diacylglycerol acyltransferase (DGAT), the primary regulators of DNL including liver X receptors (LXR), sterol regulatory element-binding protein-1c (Srebpf-1c) and carbohydrate response element binding protein (ChREBP), and cholesterol metabolism related genes such as 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), cholesterol 7 alpha-hydroxylase (Cyp7a) and LDL receptor (LDLR).
19721697	0.97	Hmg-CoA reductase (Hmgcr), SREBP-1c mainly regulates genes implicated in lipogenesis, such as the gene encoding fatty acid synthase (FAS).
25352833	0.97	fatty acid synthase (FAS), and acyl-CoA carboxylase (ACC) was detected, whereas expression of SREBP-1, SREBP-2, HMGCR, peroxisome proliferator-activated receptor alpha (PPAR-alpha), fatty acid binding protein (L-FABP), and carnitine palmitoyltransferase 1A (CPT1A) was decreased.
26023080	0.97	fatty acid synthase, stearoyl CoA desaturase 1 (Scd1), 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr) and farnesyl diphosphate synthase (Fdps), were decreased by 44-98% in streptozotocin treated mice.
26042593	0.97	Fasn, Cpt1a, Fabp4, Hmgcr and Ppara expression, while in MCS diet-fed controls Ldlr expression was significantly attenuated.
30679938	0.97	FAS and HMG-CoAR mRNA levels, which were involved in lipogenesis.
31953408	0.97	Hmgcr and farnesyl diphosphate synthase [Fds]) and fatty acid and triglyceride (TG) synthesis (fatty acid synthase [Fas], acetyl-CoA carboxylase [Acc], stearoyl-CoA desaturase-1 [Scd-1], glycerol-3-phosphate acyltransferase [Gpat]) were all significantly downregulated in the liver of gp78-/- mice (Fig. 1b).
29201040	0.96	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and fatty acid synthase (FASN), respectively.
	0.95	fatty acid synthase, tumor necrosis factor alpha, and 3-hydroxy-3-methylglutaryl-CoA reductase and the concentrations of interleukin 6 and reactive oxygen species decreased upon A. glehni.
31547031	0.96	3-hydroxy-3-methylglutaryl CoA reductase, sterol regulatory element-binding transcription factor (SREBP)-2, and low-density lipoprotein receptor, as well as fatty acid synthesis genes, such as SREBP-1c and fatty acid synthase.
	0.95	HMG-CoA reductase, SREBP1/2, FAS, and LDL receptor.
28420650	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).
31952262	0.96	FAS, SCD-1, ACC1, and HMGCR.
27499577	0.95	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.
	0.93	FAS (57%), HMGCR (78%), and increase in LDLR (50%), CYP7alpha1 (66%) and PPARalpha (75%) protein levels compared with the HFD group (Fig. 1).
	0.91	FAS, HMGCR, increasing LDLR, CYP7alpha1 and recovering adiponectin through regulating PPARs.
	0.91	FAS, HMGCR, LDLR, CYP7alpha1, PPARalpha, and adiponectin in liver and adipose tissue were recovered by PGBR.
	0.89	FAS, HMGCR, LDLR, CYP7alpha1 and PPARalpha protein expressions in liver of high-fat diet (HFD) fed mice.
	0.69	FAS, HMGCR were decreased, and
25766252	0.95	FAs including palmitic acid; and also increased the plasma total and VDLD/LDL cholesterol levels, reduced LDL receptor expression and increased HMG-CoA reductase activity.
29632203	0.95	Hmgcr, and Ldlr) while GW3965 and T0901317 activate Fasn and Srebf1 (Fig. 5B).
31993375	0.95	Hmgcr), di- and triglycerides (Plpp1, Plpp2, Plpp3, and Dgat2) and fatty acids (Fasn, Scd1, Fads1, Fads2, Elovl2, and Elovl5), and in the regulation of lipid metabolism (Srebp1c and Srebp2) was measured (Figure 7).
23945333	0.93	FASN and HMG-CoA reductase were observed in the livers of the CL-diet group.
27050512	0.92	FASN and HMGCR were unchanged in tumors of Ces3/Tgh-/- mice.
29361464	0.89	Fasn, Thrsp, and Pklr subnetworks are interconnected and partner with many lipid and cholesterol metabolism genes such as Acacb, Elovl6, Hmgcr, Mvk, Pltp, Me1, Dhcr7, and Acly, whereas Chchd6 forms a separate subnetwork surrounded by cell cycle genes as well as fatty acid related genes Cd36 and Pparg.
27912736	0.83	HMGCR, FAS and stimulated PPARalpha expressions in liver tissue compared to HC-fed groups like in vitro results.
	0.79	FAS, HMGCR and induction of PPAR-alpha hepatic protein expressions by YE in mice
19014463	0.79	Fatty acid synthase, Stearoyl CoA desaturase 1, cholesterol synthesis and uptake genes, HMG CoA reductase, LDL receptor and Egr-1 transcription factor gene, that are also activated by IGF-1 in this study.
26383020	0.78	fatty acid synthase (Fasn) involved in lipogenesis, elongation of long-chain fatty acids family member 6 and stearoyl-CoA desaturase 1 catalysing fatty acids elongation and desaturation step; Hmg-Coenzyme A synthase and Hmg-Coenzyme A reductase (Hmgcr) involved in cholesterol biosynthesis.
26322888	0.77	Hmgcr was hypermethylated (p< 0.01) but there were no methylation changes for Fasn, Nfkappab1, c-Jun, Bcl-2, and Caspase 3in HFHC group.
	0.70	Hmgcr methylation in HFHC group (p<0.01), whereas no methylation changes for Fasn, Nfkappab1, c-Jun, Bcl-2, and Caspase 3 were observed (Fig 4D).
23021221	0.75	Fasn and Hmgcr genes in cholesterol-depleted peritoneal macrophages under control, GW3965 or desmosterol treatment (6hr).
27612024	0.56	fas, and scd-1) and (C) cholesterol synthesis-related genes (srebp-2, hmgcs, and hmgcr) in different groups.