Publication for HMGCR and HMGCS1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	HMGCR	3-hydroxy-3-methylglutaryl-CoA reductase	3156			[link]
hsa	HMGCS1	3-hydroxy-3-methylglutaryl-CoA synthase 1	3157

Pubmed ID	Priority	Text
29163687	0.98	HMGCR is the key enzyme of the mevalonate pathway and these facts prompted us to investigate the mevalonate pathway enzymes HMGCS1 and HMGCR together, although the signal log ratio of HMGCR was less than 2.0 (signal log ratio=1.4).
	0.98	HMGCS1 and HMGCR in PC stroma compared with normal prostatic stroma (P<0.0001; Figs. 5, 6A and B).
	0.98	HMGCS1 and HMGCR stromal expression in PC tissues, we next analyzed the relationship between HMGCS1 or HMGCR stromal expression and the clinicopathological variables of PC specimens, which is summarized in Table IV.
	0.98	HMGCS1 as one of the candidates involved in tumor stem-like breast cancer cells, while Pandyra et al reported that dipyridamole acts as a potentiator of statin anticancer activity in multiple myeloma and acute myelogenous leukemia by attenuating the feedback response that upregulates HMGCS1 and HMGCR after statin treatment.
	0.98	HMGCS1 and HMGCR mRNAs were overexpressed in 22Rv1 cells (Fig. 3A) and their knockdown effect by shRNA was validated on mRNA level (Fig. 3B).
	0.98	HMGCS1 and HMGCR in regulating the interaction between PC and PC stroma are required, in order to fully elucidate their potential as molecular targets in the treatment of PC.
	0.97	HMGCS1 and HMGCR, respectively (Fig. 3B), and resulted in significant growth suppression as measured by both colony formation assay and MTT assay (P<0.01; Fig. 3C and D, respectively).
	0.97	HMGCS1 or HMGCR in PC stromal cells was found to induce a significantly higher growth rate of 22Rv1 cells than those that were mock transfected (P<0.01; Fig. 4), indicating a paracrine effect.
	0.97	HMGCS1 or anti-HMGCR antibodies.
	0.97	HMGCS1 and HMGCR using clinical PC specimens in this study, since PC specimens showed apparent stromal expression of HMGCS1 and HMGCR (Fig. 5).
	0.97	HMGCS1 and HMGCR is likely to be involved in PC cell growth through an autocrine/paracrine mechanism, supporting their potential of these proteins as molecular targets for PC therapy.
	0.97	HMGCS1 and HMGCR were overexpressed in 22Rv1 cells, compared with normal prostate cells.
	0.96	HMGCS1 and HMGCR have an influence on survival or progression of PC patients in the future study.
	0.95	HMGCS1 and HMGCR stromal overexpression might be key factor in regulating the transition from organ-confined to metastatic disease in PC.
	0.94	HMGCS1 and HMGCR.
	0.93	HMGCS1 and HMGCR were the upregulated genes in stroma, those were not among the genes in Tables II and III, which were derived from PC and epithelium.
	0.93	HMGCS1 and HMGCR may similarly represent molecular targets for the treatment of PC.
	0.92	HMGCR, although there are no studies available on HMGCS1.
	0.91	HMGCS1, 3-hydroxy-3-methylglutaryl-CoA synthase 1; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; RT-PCR, reverse transcription-polymerase chain reaction; PC, prostate cancer.
	0.90	HMGCS1 condenses acetyl-CoA with acetoacetyl-CoA to form HMG-CoA, which is the substrate for HMGCR.
	0.89	HMGCS1 and HMGCR were overexpressed in PC stroma, especially in early stage PC.
	0.89	HMGCS1, 3-hydroxy-3-methylglutaryl-CoA synthase 1; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase.
	0.88	HMGCS1 or HMGCR stromal expression and Gleason grade, tumor classification, or PSA expression levels (data not shown).
	0.85	HMGCS1 or HMGCR overexpression promotes PC cell proliferation through autocrine/paracrine regulation
	0.85	HMGCS1 or HMGCR stromal expression.
	0.84	HMGCS1 and HMGCR in PC, as well as in PC stroma, might serve as molecular targets for the treatment of PC.
	0.84	HMGCS1 or HMGCR was associated with less aggressive PC (Fig. 6C-H).
	0.84	HMGCS1 and HMGCR might be needed for PC growth until PC progresses to aggressive disease, and then downregulated once PC invasion or metastasis has been developed.
	0.77	HMGCS1 or HMGCR in either PC cells or prostate stromal cells stimulated PC cell growth, suggesting a possible autocrine/paracrine mechanism of action.
	0.77	HMGCS1 and HMGCR.
	0.73	HMGCS1- or HMGCR-overexpressing PrSC cells (transfected with HMGCS1 or HMGCR expression vectors), grew more rapidly than those co-cultured with PrSC mock transfectants.
	0.70	HMGCS1 and HMGCR in PC stroma.
	0.63	HMGCS1 or HMGCR expression by shRNA attenuates PC cell viability.
30537987	0.98	HMG-CoA reductase (HMGCR) and HMG-CoA synthase 1(HMGCS1), key enzymes in the cholesterol biosynthesis pathway, were deregulated in the normal-to-preneoplastic transition.
	0.98	HMGCR and HMGCS1 are regulated by miR-140-3p-1, we restored levels of these in the preneoplastic MCF10.AT1 cell line by transfecting cells with miR-140-3p-1 mimic.
	0.98	HMGCR and HMGCS1 and represses their activity.
	0.97	HMGCR or HMGCS1 reporter along with the miR-140-3p-1/scramble mimic.
	0.96	HMGCR and HMGCS1.
	0.93	HMGCR and HMGCS1 3' UTR) by 55% (Fig. 3c).
	0.91	HMGCR or HMGCS1.
	0.91	HMGCR and HMGCS1 transcripts in the MCF10A progression model using qPCR.
	0.90	HMGCR and HMGCS1, with the loss of miR-140-3p-1 promoting upregulation of HMGCR and HMGCS1 during the multi-step tumorigenic process.
	0.89	HMGCR and HMGCS1, was the top predicted pathway to be deregulated (Additional file 3: Figure S2 B).
	0.89	HMGCR and HMGCS1 were repressed (by 37% and 47%) with the addition of miR-140-3p-1 mimic relative to their expression upon transfection of scramble control mimic, confirming this predicted miR-gene relationship to be valid in the context of breast preneoplastic cells (Fig. 3a).
	0.84	HMG-COA reductase (HMGCR) and HMG-COA synthase1 (HMGCS1) are directly regulated by miR-140-3p-1.
	0.84	HMGCR (about 2.5-fold) and HMGCS1 (5.5-fold) in the cell lines from later stages of tumorigenic progression compared to the normal-like MCF10A(P) cell line (Additional file 3: Figure S2 C&D).
	0.82	HMGCR and HMGCS1, suggesting that other mechanisms must be at play that have activated MVA pathway in our system.
25933205	0.98	HMGCR and HMGCS target genes were significantly up-regulated by TSH in HepG2 cells, which was consistent with our previous findings.
	0.97	HMGCR was also significantly reduced, and HMGCS mRNA expression exhibited a decreasing trend (Fig 3B).
	0.95	3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and low-density lipoprotein receptor (LDLR).
	0.95	HMGCR and HMGCS.
	0.93	HMGCR and HMGCS, which are key enzymes in cholesterol biosynthesis, and suppressed the TSH-stimulated up-regulation of SREBP-2 in HepG2 cells; similar results were obtained in TSH receptor knockout mice.
	0.91	HMGCR mRNA expression and a slight decrease in HMGCS mRNA expression; this disparity may derive from the differential effects of SREBP-2 in stimulating target gene transcription.
	0.84	HMGCR and HMGCS in HepG2 cells.
	0.82	HMGCS mRNA expression at 48 h and HMGCR mRNA expression at both 24 and 48 h (p<0.05) (Fig 1D).
	0.74	HMGCR and HMGCS.
	0.55	HMGCR and HMGCS mRNA expression was attenuated by AICAR in HepG2 cells (Fig 4E).
26535009	0.98	HMGCR, HMGCS1, DHCR7, DHCR24, LDLR, FDFT1, FDPS, IDI1, MVD, SQLE, LSS, NSDHL, SC5DL, INSIG1, ACLY, and ACSS2 (see fig. S1 for full list).
	0.98	HMGCR, HMGCS1, and LDLR mRNA an additional 2- to 3-fold (fig. S3A).
	0.98	HMGCR, HMGCS1, or LDLR in T47D cells incubated in LPDS for 24 hours followed by concomitant NRG1 (50 ng/ml) treatment for the final 2 hours.
	0.97	HMGCR, HMGCS1, and LDLR beyond amounts induced through lipoprotein depletion.
	0.87	HMGCR, HMGCS1, and LDLR) .
	0.79	HMGCR 2-fold, HMGCS1 2-fold, and LDLR 3-fold (Fig. 2A).
	0.74	HMGCR or HMGCS1 mRNA in the presence of ERBB4.
	0.65	HMGCR, and HMGCS1 mRNA expression in MCF10A pINDUCER20 ERBB4 JM-a CYT-2 cells in the absence or presence of DOX (fig. S6A, S6B).
	0.54	HMGCR, HMGCS1, and LDLR) and increased LDL uptake and cholesterol synthesis.
21408089	0.98	HMGCS1, HMGCR, and SQLE (Figure 2A).
	0.94	Hmgcs1, Hmgcr, Idi1, and Sqle was measured by qRT-PCR.
	0.93	Hmgcs1, Hmgcr, Idi1, and Sqle genes in BMDM infected with mCMV(24 hpi) (C) or treated for 24 h with IFNgamma (10 and 100 U/ml) (D), IFNbeta (10 and 25 U/ml) (E), IL6 (10 and 25 U/ml) (F), IL1beta (10 and 100 U/ml) (G), or TNF (10 and 100 U/ml) (H).
	0.92	Hmgcs1, Hmgcr, IdI1, and Sqle:shows a statistically significant but quantitatively modest reduction in expression (Figure 1C and 1D).
	0.92	Hmgcs1, Hmgcr, Idi1, and Sqle gene expression changes were then analyzed by Q-RT-PCR (Figure 1E-H).
	0.91	Hmgcs1, Hmgcr, Idi1, and Sqle genes in BMDM after 24 h mock treatment, mCMV, or mCMVdie3 infection, respectively.
	0.83	HMGCS1, HMGCR, and SQLE protein levels in mCMV infected (24 hpi) or mock-treated BMDM.
	0.70	HMGCS1, 50% for HMGCR, and 85% for SQLE.
26353928	0.98	HMGCS1 and HMGCR.
	0.97	HMGCR and HMGCS1.
	0.94	HMGCR and HMGCS1 was accompanied by increased SREBP2 cleavage in the shControl lines (Figure 6C).
	0.92	HMGCR (A), HMGCS1 (B) relative to GAPDH in shMCF7 cell lines.
	0.88	HMGCS1, GGPS1 and SREBP2 knockdown, in concert with statin-mediated HMGCR inhibition, can robustly enhance tumor cell apoptosis.
	0.82	HMGCR and HMGCS1 in response to fluvastatin treatment.
	0.60	HMGCR and HMGCS1.
31685796	0.98	HMG-CoA reductase (HMGCR) and HMG-CoA synthase1 (HMGCS1), which are the rate-limiting enzymes for mevalonate pathway, by real-time PCR and Western Blotting.
	0.97	HMGCS1 and HMGCR in HCC-LM3 and HepG2 cells.
	0.97	HMGCR and HMGCS1 protein in HCC-LM3 cells infected with LV-shASPP2 or LV-shNon and treated with siAspp2 and/or siSrebp2.
	0.92	HMGCR and HMGCS-1 expression were ablated when Srebp-2 was knocked down (Fig. 4f).
	0.91	HMGCR and HMGCS-1 expression (Fig. 3c).
	0.90	HMGCR and HMGCS-1 expression.
26548416	0.98	Hmgcr, Hmgcs1, Sqle, Nsdhl, Cyp51 and Egr1) (Fig. 3).
	0.97	HMGCR, HMGCS1, CYP51, NSDHL, SQLE and SREBP1) was significantly reduced upon treatment with metformin (Fig. 5).
	0.94	Hmgcr, Hmgcs1, Nsdhl, Cyp51).
	0.82	Hmgcr and Hmgcs1).
31561416	0.98	HMGCS1, HMGCR, MVD, and FDPS, in order to increase intracellular cholesterol levels.
	0.98	HMGCR, HMGCS1, and SREBP2 was observed in UA-treated SK-HEP1 and Hep3B cells (Figure 2B).
	0.96	HMGCS1), HMG-CoA reductase (HMGCR), farnesyl diphosphate synthase (FDPS), and mevalonate diphosphate decarboxylase (MVD), for de novo cholesterol synthesis.
	0.96	HMGCS1, HMGCR, MVD, FDPS, and SREBP2), fatty acid synthesis (SREBP1a and SREBP1c), and cholesterol uptake (LDL-R) in UA-treated SK-HEP-1 cells, and this UA-induced gene expression was similar to that observed with simvastatin treatment (Figure 2A).
22162773	0.98	HMGCR, HMGCS1 and IDI1.
	0.82	HMGCS1 levels, 0.94, 1.8 and 2.4 (p value = 0.03) fold increase in HMGCR levels, 1.6, 2.4 and 2.5 (p value = 0.024) fold increase in IDI1 levels at 24 h, 48 h and 72 h post transfection, respectively Non significant changes were observed in case of cells transfected with scrambled siRNA (Fig. 3e).
	0.57	HMGCR, HMGCS1 and IDI1 (genes of the cholesterol synthesis pathway).
22754327	0.98	3'-hydroxylmethyl glutaryl coenzyme A synthase (HMGCS) and 3'-hydroxylmethyl glutaryl coenzyme A reductase (HMGCR).
	0.85	HMGCS and HMGCR are major enzymes in hepatic cholesterol biosynthesis.
	0.83	HMGCS and HMGCR, then down-regulates cholesterol biosynthesis in the liver.
24829397	0.98	HMGCR, HMGCS1, LDLR, DHCR7), and cytokines (IL8, CCL20, CXCL1).
	0.98	HMGCR and HMGCS1 are regulated by PPARalpha, whose activity is modulated by NCOR1, known to form a nuclear complex with ERBB4.
	0.94	HMGCR, HMGCS1, TP63, and KRT14, all of which were upregulated except for SPARC, which was reduced with ERBB4 expression (Figure 5B).
26938778	0.98	HMGCS1 (Entrez Gene: 208715), HMGCR (Entrez Gene: 15357), MVD (Entrez Gene: 192156), SQLE (Entrez Gene: 20775), and SREBF2 (Entrez Gene: 20788) in CH25H -/- cells treated with interferon gamma (IFN-gamma) (UniProt: P01580).
	0.92	HMGCR, SQLE and SREBF2) and 24 h (HMGCS1, HMGCR, MVD and SQLE) after addition of the cytokine.
	0.90	HMGCS1 (-32%), HMGCR (-51%), MVD (-48%), SQLE (-51%) and NSDHL (Entrez Gene: 18194) (-62%) relative to cells treated with the nontargeting control (Fig 7A).
27308369	0.98	HMGCR inhibition (1), depletion of cholesterol and other sterol intermediates causes translocation of SREBP2 into the nucleus (2), and the ensuing transcription of sterol-responsive genes including HMGCR, HMGCS1, and LDLR, thereby blunting the anticancer efficacy of statins in tumor cells (3).
	0.98	HMGCR, 3-hydroxy-3-methylglutaryl coenzyme A reductase; HMGCS1, HMG-CoA synthase 1; SREBP2, sterol regulatory element binding transcription factor 2; FPP, farnesyl pyrophosphate; GGPP, geranaylgeranyl pyrophosphate; LDLr, low-density lipoprotein receptor.
	0.98	HMGCR, HMG-CoA synthase 1 (HMGCS1), and low-density lipoprotein receptor (LDLr) (Fig. 1B).
27705805	0.98	HMGCS1 (catalyzing HMG-CoA synthesis), HMGCR (rate-limiting enzyme of the cholesterol pathway), SQLE (catalyzing the first cholesterol-specific step in the cholesterol pathway), PHGDH and PSAT1 (the first two enzymes in the serine-glycine pathway), and SHMT2 (linking glycine synthesis to one-carbon metabolism and nucleotide production).
	0.97	Hmgcs1, Hmgcr, Mvk, Phgdh, Psat1, Psph, and Shmt2 (Figure 3E).
	0.96	Hmgcs1, Hmgcr, Mvk, Phgdh, Psat1, Psph, and Shmt2 (Figure 3F).
31138790	0.98	HMGCS1, HMGCR and DHCR24 between ccRCC and adjacent tissues in the TCGA database.
	0.98	HMGCS1 and HMGCR was lower in ccRCC cells than in adjacent tissues, and thus, we concluded that the cause of the higher cholesterol content in ccRCC is not cholesterol synthesis but exogenous uptake.
	0.97	HMGCS1, HMGCR and DHCR24 gene expression was low in ccRCC cells (Fig. 6c), which indicated that ccRCC cells do not acquire cholesterol through synthesis.
31490950	0.98	hmgcs1, hmgcr, fdft1, sqle, and cyp51 was done using RNA isolated from OPCs induced to differentiate in OPC media with the addition of T3 45nM (Black), Quetiapine 1muM (Blue), or both (Grey) at 48 and 96 hrs.
	0.97	hmgcs1, hmgcr, fdft1, cyp51, and sqle, are induced by T3 and quetiapine or quetiapine alone.
	0.70	hmgcs1, hmgcr, fdft1, sqle, cyp51 by qPCR analysis.
31932581	0.98	HMGCS1 and HMGCR in A2780 and SKOV3 cells with treatment as indicated.
	0.89	HMGCS1 and HMGCR in A2780 and SKOV3 cells with treatment as indicated.
	0.50	HMGCS1, HMGCR).
19560108	0.98	3-hydroxy-methylglutaryl-CoA reductase (HMGCR), 3-hydroxy-methylglutaryl-CoA synthase 1 (HMGCS), emopamil sterol isomerase (EBP), squalene epoxidase (SQLE) and sterol 4 methyl oxidase (SCAMOL).
	0.81	HMGCS and HMGCR was activated 1.5 to 2.7-fold (p<0.001) by culture of freshly isolated trophoblast cells in the presence of 400 nMol/L oleate but not with 10 mMol/L glucose (Figure 4).
29703166	0.98	HMGCR and SQLE (rate limiting enzymes), FDFT1, LSS (catalyzes first step), DHCR7 (catalyzes last step) in addition to NSDHL, MDMO1, EBP, IDI1, CYP51A1, HMGCS1 and SC5D.
	0.94	HMGCS1, HMGCR, IDI1, FDFT1, SQLE, CYP51A1, MSMO1, NSDHL, EBP and SC5D) ranked among the top 150 most differentially expressed genes in the balanced dataset (average rank of 76) (Additional file 2).
30561264	0.98	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR; 3.5- and 4-fold, respectively), 3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1; 5.5- and 6.5-fold, respectively), low-density lipoprotein receptor (LDLR; 3.5- and 2-fold, respectively), and proprotein convertase subtilisin/kexin type 9 (PCSK9; 3.5- and 2-fold, respectively; Figure 8A and Table 3).
	0.94	HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; HMGCS1, 3-hydroxy-3-methylglutaryl-CoA synthase 1; LCAT, lecithin-cholesterol acyltransferase; LDLR, low-density lipoprotein receptor; LSD, least significant difference; MTTP, microsomal triglyceride transfer protein; NPC1L1, NPC1 like intracellular cholesterol transporter 1; PCSK9, proprotein convertase subtilisin/kexin type 9; SOAT2, sterol O-acyltransferase 2; SREBF2, sterol regulatory element binding transcription factor 2.
18959802	0.98	Hmgcr, Hmgcs1, Srebf2, Fabp Fasn, Fdps, Acaca, Acadm, Acat2, ApoA5, C1, E and L1 as well as Cyp27a1, Ldlr, Ppargamma and Tyms (Figure 4).
20531405	0.98	HMGCR and HMGCS, as well as many other SREBP2-dependent genes.
22265415	0.98	HMGCS1 (HR = 1.21, q = 0.007), HMGCR (HR = 1.17, q = 0.032), IDI1 (HR = 1.26, q < 0.001), FDPS (HR = 1.17, q = 0.012), SQLE (HR = 1.35, q < 0.001), LSS (HR = 1.16, q = 0.032), NSDHL (HR = 1.17, q = 0.032), DHCR7 (HR = 1.26, q < 0.001).
24619155	0.98	HMGCR, HMGCS, and LDLR in NPC1 cells were evaluated after treatment with HE-SS-PRX or HP-beta-CD (Fig. 4B).
25763114	0.98	HMGCS1) (Figure 2B; P < 0.001) and the rate limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) (Figure 2C; P < 0.01) was significantly upregulated in NoB and LB condition compared to control.
26512780	0.98	3-hydroxy-3-methyl-glutaryl-CoA synthase 1 (HMGCS1), HMGCR, mevalonate kinase (MVK), mevalonate 5-pyrophosphate decarboxylase (MVD) and low-density lipoprotein receptor (LDLR) for cholesterogenesis; and two chaperones, insulin-induced gene 1 (INSIG1) and SREBP cleavage activating protein (SCAP) in PC-3 EV, PC-3 R248W and DU145 cells.
27654507	0.98	HMGCR, SQLE, and HMGCS1) have been reported to undergo ubiquitin-regulated proteasomal degradation.
28357032	0.98	HMGCS1, HMGCR, SQLE, CYP7A1 and LDLR.
30584280	0.97	HMGCR and HMGCS in HepG2 cells.
	0.97	HMGCR, HMGCS, LDLR, and GAPDH protein levels were measured by WB.
	0.96	HMGCR and HMGCS protein levels.
	0.94	3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), and low-density lipoprotein receptor (LDLR).
	0.93	HMGCR and HMGCS by metformin treatment.
	0.89	HMGCR and HMGCS; DN-AMPK attenuated the cholesterol-lowering effect of metformin, which is obvious evidence suggesting that metformin effects are primarily mediated by AMPK.
32028644	0.97	HMGCR and HMGCS1, was also increased after BIX treatment in A549 (Figure 4E).
	0.96	HMGCR (B), and HMGCS1 (C) was analyzed in BIX- and 25-hydroxycholesterol (25-HC)-treated H1299 cells.
	0.93	HMGCR, and HMGCS1, while in contrast, their expressions were significantly reduced by the 25-HC treatment (Figure 5A-C).
	0.87	HMGCR and HMGCS1, which are the rate-limiting step of cholesterol biosynthesis, was verified by qRT-PCR.
	0.60	HMGCR and HMGCS1.
	0.57	HMGCR and HMGCS1 increased significantly after BIX treatment (Figure 4C).
21559365	0.97	HMGCR splice variants, we tested whether there are also sterol-regulated changes in the relative amounts of alternatively spliced to full-length transcripts of other key regulatory genes involved in cholesterol metabolism - LDLR, HMGCS1, MVK, and PCSK9.
	0.97	HMGCS1, HMGCR, MVK, LDLR and PCSK9 with cDNA derived the liver of an African Green monkey or HepG2 cell line (human control).
	0.96	HMGCR, LDLR, HMGCS1, MVK and PCSK9 are among the genes whose transcription is regulated in a coordinated fashion by SREBP in response to sterols, we sought to determine if the relative levels of the alternatively spliced versus full-length transcripts are also subject to sterol regulation.
	0.95	HMGCS1), which catalyzes the reaction immediately before HMGCR, has a highly complex 5' UTR that regulates translational efficiency and undergoes exon 2 skipping.
	0.95	HMGCR, LDLR, HMGCS1, MVK and PCSK9 in hepatocytes (HepG2), human immortalized lymphoblast cell lines, and livers from cholesterol-fed African Green monkeys, are reduced under conditions of sterol depletion, and induced under conditions of sterol loading.
31651237	0.97	HMGCS1, INSIG1, LPIN1, HMGCR, and ACSS2 were found to be significantly upregulated in comparison groups Mock vs. MBV6h, Mock vs. MBV 12 h, and Mock vs. MBV24h groups.
	0.97	HMGCS1, FDFT1, HMGCR, and ACSS2 were found to play important roles in maintaining the tight connection of the whole network.
	0.96	HMGCS1, FDFT1, HMGCR, and ACSS2 were associated with lipid synthesis and metabolism, thereby suggesting that BVDV infection induced lipid synthesis and metabolism activity in host cells.
	0.90	HMGCR, HMGCS1, and LPIN1 were also validated by RT-qPCR (Fig. 7).
	0.52	HMGCR, HMGCS1, LPIN1, validated by RT-qPCR.
24493696	0.97	HMGCS1, HMGCR, MVK, MVD and LDLR, and further reduces the levels of intracellular fatty acid and cholesterol.
	0.96	HMGCS1, HMGCR, MVK, MVD and LDLR and two chaperones, INSIG-1 and SCAP in LNCaP and C4-2B cells examined by qRT-PCR.
	0.93	HMGCS1, HMGCR, MVK, MVD, INSIG1 and SCAP (Fig. 5A).
	0.75	HMGCS1, HMGCR, MVK, MVD and LDLR for cholesterogenesis, two chaperones, INSIG1 and SCAP.
30321984	0.97	HMGCS1), HMG-CoA reductase (HMGCR), farnesyl diphosphate synthase (FDPS), and mevalonate diphosphate decarboxylase (MVD).
	0.96	HMGCS1, HMGCR, and FDPS, were decreased by emodin in SK-HEP-1 cells in a dose-dependent manner (Figure 4D).
	0.95	HMGCS1, HMGCR, FDPS, DHCR7, and DHCR24 after treatment of HCC cells with emodin and sorafenib.
	0.93	HMGCS1, HMGCR, mevalonate diphosphate decarboxylase (MVD), FDPS, and 7-dehydrocholesterol reductase (DHCR7) expression, by simvastatin was significantly decreased by 20 muM emodin in SK-HEP-1 (Figure 4B) and HepG2 (Figure 4C) cells.
30975976	0.97	HMGCS1, HMGCR, beta-catenin, and YAP than paracarcinoma tissue.
	0.97	HMGCS1 and HMGCR in the cancer tissue is much higher than in the paracarcinoma tissue, which is consistent with a recent report by Deng et al..
	0.95	HMGCR and HMGCS1.
	0.90	HMGCS1, HMGCR, beta-catenin, TAZ, CTGF, and CYR61 than paracarcinoma tissue.
20110263	0.97	HMGCS1, HMGCR, FDFT1, SC4MOL and LPIN1 genes.
	0.81	HMGCS1, HMGCR, FDFT1, SC4MOL, and LPIN1, expression of which was induced by GW7647, suggesting cross-talk between PPARalpha and SREBP signaling.
23324130	0.97	HMGCS1, INSIG1 moderately up-regulated and HMGCR highly up-regulated.
	0.97	HMG-CoA synthetase (HMGCS), conversion of acetyl-CoA and acetoacetyl-CoA to 3-hydroxy-3-methylglutaryl- CoA (HMG-CoA) and subsequent HMG-CoA reductase (HMGCR) catalysis of the rate-limiting step in cholesterol biosynthesis by converting HMG-CoA to mevalonate (Figure 4C).
25313139	0.97	HMGCS and HMGCR) by orlistat and TOFA but not TCS and C75.
	0.60	hydroxy-methyl-glutaryl-CoA synthase (HMGCS) and hydroxy-methyl-glutaryl-CoA reductase (HMGCR), two key enzymes of cholesterol synthesis.
28698273	0.97	HMGCS1, the enzyme immediately upstream of HMGCR in the mevalonate pathway.
	0.96	HMGCS1 and HMGCR 3' UTRs perturbed cholesterol levels (Fig. 3A).
32161285	0.97	hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and HMGC synthase (HMGCS).
	0.74	HMGCR and HMGCS, but had no effect on expression of genes involved in SREBP2 maturation, including SCAP and PAQR3 (Fig. 4f).
20338039	0.97	HMGCS1 (cytosolic HMG-CoA synthase); HMGCR (HMG-CoA reductase); FDPS (farnesyl diphosphate synthase); FDFT1 (farnesyl-diphosphate farnesyltransferase 1, also known as squalene synthase); LDLR (low-density lipoprotein receptor).
25563794	0.97	HMGCS, HMGCR, LDLR, farnesyl diphosphate synthase, and squalene synthase.
31497741	0.97	HMGCR, 3-hydroxy-3-methylglutaryl coenzyme A synthase (HMGCS), and LDLR.39 In line with the TC and FC accumulation, our gene and protein analysis revealed that the I148M PNPLA3-carrying HSCs displayed lower SREBP-2 transcriptional activity in both primary and overexpressing cells, as suggested by decreased LDLR, HMGCR, and HMGCS expressions (Fig. 2D,E; Supporting Figs. S1 and S2).
31604910	0.97	HMGCS1, HMGCR, MVK, and SQLE (Fig. 3e).
31023626	0.96	HMGCR results in the cleavage and activation of SREBP2 and upregulation of the MVA pathway enzymes HMGCR and HMGCS1.
	0.96	HMGCR and HMGCS1 expression by qRT-PCR.
	0.96	HMGCR and HMGCS1 mRNA expression (Figure 3F).
	0.92	HMGCR, HMGCS1, INSIG1 and SCD expression by qRT-PCR.
	0.91	HMGCR and HMGCS1 expression in response to fluvastatin was not due to a lack of SREBP2 expression (Figure 3D).
32034223	0.96	HMGCR, HMGCS, and LDLR were examined in primary human myoblasts undergoing differentiation under statin treatment (5 microM) for 72 h-96 h. The results were normalized to two reference genes and calculated relatively to DMSO-treated samples.
	0.96	HMGCR, HMGCS1, LDLR, and PCSK9 are increased under statin treatment in primary human muscle cells.
	0.95	HMGCS1, HMGCR, CYP51A1, 7-dehydrocholesterol reductase DHCR7) as well as cholesterol transport (low density lipoprotein receptor LDLR, ATP-binding cassette transporter ABCA1 and ABCG1) expressed in human muscle cells and significantly altered by different exposure to statins.
	0.94	HMGCS and HMGCR (Fig. 2D), the same effects that have been described for liver including LDL receptor.
	0.94	HMGCS1, HMGCR, CYP51A1, DHCR7) and transport (i.e. ABCA1, ABCG1, LDLR).
26535575	0.96	HMGCS1, TM7SF2, FDFT1, EBP, FDPS, HMGCR, SQLE, and DHCR7.
	0.95	HMGCS1, FDPS, HMGCR, and ACAT2.
	0.92	HMGCS1, TMEM97, TM7SF2, FDFT1, ACAT2, EBP, FDPS, HMGCR, SQLE, DHCR7, C14orf1, and INSIG1.
31225926	0.96	HMGCS1, the enyzme HMGCR converts HMG-CoA to mevalonate.
31540279	0.95	3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1), fatty acid synthase (FASN), and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), in HepG2 cells.
	0.91	HMGCS1, mevalonate diphosphate decarboxylase (MVD), and HMGCR in simvastatin-treated SK-HEP-1 cells (Figure 3B).
	0.89	3-Hydroxy-3-Methylglutaryl-CoA Synthase 1 (HMGCS1), 3-Hydroxy-3-Methylglutaryl-CoA Reductase (HMGCR), farnesyl diphosphate synthase (FDPS), and mevalonate diphosphate decarboxylase (MVD).
29290960	0.95	HMGCS1 might be is rapidly converted to MVA by HMGCR in Cisplatin-resistant cells.
	0.87	HMGCS1 and HMGCR was higher in Cisplatin-resistant cells than in the parental cells, but the amount of HMG-CoA was almost the same between these cell lines.
27648077	0.95	3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1), HMG-CoA reductase (HMGCR), farnesyl diphosphate synthase (FDPS), Cytochrome P450 Family 51 Subfamily A Polypeptide 1 (CYP51A1), and 7-dehydrocholesterol reductase (DHCR7) mRNA levels (Figure 5(b)).
29493120	0.94	HMGCS and HMGCR convert acetyl-CoA to 3-hydroxyl-3-3-methylglutaryl-CoA and mevalonate, respectively) and the lower mevalonate pathway (a series of enzymes that catalyze mevalonate to cholesterol).
	0.92	HMGCS and HMGCR do not promote GCa progression, which explains the failure of clinical trials of statin in GCa patients.
	0.90	HMGCS and HMGCR, which is a pharmacological target site of statins (cholesterol-lowering drugs).
	0.77	HMGCS and HMGCR are negatively associated with GCa progression (Fig. 2B; HR score = -60.8 and -356.5, respectively).
23919967	0.94	HMGCS, FDPS, HMGCR, STAR, and CYP11A1 were all elevated in C81 relative to C33 cells.
	0.91	HMGCS, FDPS, and HMGCR), and an elevated cholesterol synthesis measured via 13C acetate incorporation into newly synthesiszed cholesterol.
23990020	0.94	HMGCS1, HMGCR, LDLR) as its targets might also control a miR-128-2 that is not only pro-apoptotic but also regulates cholesterol metabolism in harmony with SREBP2.
29712938	0.94	HMGCR, SQLE, 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 1 (HMGCS1), CETP, and PCSK9, which are regulated by SREBP-2, might be responsible for cholesterol lowering effects by sauchinone.
31316083	0.93	HMGCS1 and HMGCR, two rate-limiting enzymes in the de novo cholesterol synthesis (DNCS) pathway in melanomas.
20811644	0.92	HMGCS is regulated by SREBP2 rather than SREBP1 and like HMGR plays a role in cholesterol synthesis.
31969805	0.92	HMGCS-1 and the HMG-CoA reductase HMGCR mediate this pathway as mentioned above, whereas stains as cholesterol-lowering drugs act by inhibiting the HMGCR.
28910500	0.91	HMGCS1 describe results obtained from experiments with HMGCR (Balasubramanian et al., 1989).
31098406	0.87	HMGCR, HMGCS1, and FPP) can be abolished by the minimal effective dose of 0.5 mug mL-1 25-HC (Fig. 5a), supporting the view that activation of SREBP2 is a feedback consequence of sterol deficiency caused by HTE treatment.
	0.51	HMGCS1, HMGCR, and FPP) in HepG2 cells (n = 3).
22002007	0.87	Hmgcr with palmitate, the expression of other SREBP-1-regulated genes (e.g. Acaca, Fasn and Hmgcs1) did not consistently follow the same pattern of expression (ESM Fig. 3).
24203995	0.87	HMGCS and HMGCR, respectively).
26646011	0.86	HMGCS1, HMG-CoA synthase 1; HMGCR, HMG-CoA reductase; FDPS, farnesyl diphosphate synthase; SQLE, squalene epoxidase; LSS, lanosterol synthase; NSDHL, NAD(P)-dependent steroid dehydrogenase-like; DHCR24, 24-dehydrocholesterol reductase; SC5D, sterol-C5-desaturase; DHCR7, 7-dehydrocholesterol reductase.
	0.51	HMGCS1, HMG-CoA synthase 1; HMGCR, HMG-CoA reductase; MVK, mevalonate kinase; PMVK, phosphomevalonate kinase; MVD, mevalonate decarboxylase; IDI1, isopentenyl-diphosphate delta isomerase 1; FDPS, farnesyl diphosphate synthase; FDFT1, farnesyl-diphosphate farnesyltransferase 1; SQLE, squalene epoxidase; LSS, lanosterol synthase; CYP51A1, cytochrome P450 family 41 subfamily A; TM7SF2, transmembrane 7 superfamily member 2; NSDHL, NAD(P)-dependent steroid dehydrogenase-like; HSD17B7, hydroxysteroid 17-beta dehydrogenase; DHCR24, 24-dehydrocholesterol reductase; SC5D, sterol-C5-desaturase; DHCR7, 7-dehydrocholesterol reductase.
20947216	0.85	HMGCR and HMGCS were not significantly reduced by MK-801.
31518366	0.83	HMGCS1, which condenses acetoacetyl-CoA and acetyl-CoA to produce 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA), and the rate-limiting pathway enzyme HMG-CoA reductase (HMGCR) were strongly upregulated even by 2 days post-infection (DPI), prior to the onset of cell proliferation.
17052361	0.80	HMGCS1 and HMGCR.
	0.60	HMGCS1, HMGCR, FDPS, SC5DL and DHCR7; see legend to Fig. 1 for complete names), cholesterol transport (LDLR) and fatty acid biosynthesis (FASN and SCD1).
31159817	0.79	HMGCR, HMGCS1, FDPS, LSS and SQLE) and lipogenic (e.g. ACACA, SCD, FASN, FADS1 and ELOVL6) pathways.
31181660	0.70	HMGCS1), 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR), Mevalonate kinases (MVK), Phosphomevalonate Kinase (PMVK), Mevalonate Diphosphate Decarboxylase (MVD), 7-Dehydrocholesterol reductase (DHCR7)) (Figure 1c and Figure S1d).
29226804	0.67	HMGCS1 activity did not activate SREBP2 indicated that HMGCS1 is not a rate-limiting enzyme in this pathway, a finding in agreement with the general view that HMGCR catalyzes the committing and first rate-limiting step.
30634538	0.65	3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) and microsomal TG transfer protein (MTTP), 3-hydroxy-3-methylglutaryl-coenzyme A synthase 1 (HMGCS1).