Publication for HMGCS1 and LDLR

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	HMGCS1	3-hydroxy-3-methylglutaryl-CoA synthase 1	3157			[link]
hsa	LDLR	low density lipoprotein receptor	3949

Pubmed ID	Priority	Text
28526856	0.98	HMGCS, LDLr) and efflux (ABCA1, ABCG1, ABCG5, NPC1, NPC2) gene expression.
	0.96	HMGCS were all upregulated 2.5-3-fold (P < 0.001), while LDLr was upregulated nearly 5-fold (P < 0.001, Fig. 3).
30700717	0.98	LDLr, HMGCS1, FDFT1 and DHCR7 messenger RNA (mRNA) levels (n = 6-7).
	0.92	LDLR, HMGCS1, FDFT1 and DHCR7 were downregulated at the mRNA level in a dose-dependent manner when cells were exposed to 25-HC for the 36 h incubation period (Fig. 4a).
32034223	0.98	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.
	0.94	HMGCS and HMGCR (Fig. 2D), the same effects that have been described for liver including LDL receptor.
21559365	0.97	LDLR, HMGCS1 and MVK.
	0.96	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.
	0.96	HMGCS1 2(+), MVK4(+), LDLR4(+), LDLR12(+) and PCSK9 8(+) transcripts in liver biopsies of monkeys fed either a cholesterol-supplemented or control diet.
	0.96	HMGCS1, MVK, LDLR and PCSK9 transcripts were quantified in liver biopsies obtained from monkeys with (n = 28) and without (n = 23) cholesterol supplementation.
	0.95	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, HMGCR, MVK, LDLR and PCSK9 with cDNA derived the liver of an African Green monkey or HepG2 cell line (human control).
	0.94	LDLR12(-), HMGCS1 2(-), MVK4(-), and PCSK9 8(-) by 9-23%, (p<0.05, Figure 7B ).
	0.79	HMGCS1, LDLR and MVK were reduced in the cells transfected with the non-targeting siRNA after sterol depletion, but not after PTBP1 knock-down.
26535009	0.97	HMG-CoA-Synthase 1 (HMGCS1), and Low-Density Lipoprotein Receptor (LDLR) .
	0.96	HMGCS1, DHCR7, DHCR24, LDLR, FDFT1, FDPS, IDI1, MVD, SQLE, LSS, NSDHL, SC5DL, INSIG1, ACLY, and ACSS2 (see fig. S1 for full list).
	0.96	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.
	0.89	LDLR, HMGCR, and HMGCS1 mRNA expression in MCF10A pINDUCER20 ERBB4 JM-a CYT-2 cells in the absence or presence of DOX (fig. S6A, S6B).
	0.73	HMGCS1, and LDLR) .
20811644	0.97	LDLR transcription by 26%+-11%, but decreases HMGCS transcription by 13%+-3% ( Fig 4d ).
	0.92	LDLR transcription by 26% (p = 0.02) while inhibiting HMGCS transcription by 13% (p = 0.001).
	0.88	LDLR and HMGCS promoters in Huh7 cells using reporter constructs.
23314925	0.97	HMGCS1, MVK, LDLR and PCSK9, consistent with the likelihood that these changes are mediated at least in part by sterol regulation of PTBP1.
	0.96	LDLR, MVK, HMGCS1 and PSCK9.
	0.95	LDLR, MVK, HMGCS1 and PSCK9 but did not appear to regulate HMGCR exon 13 alternative splicing.
24493696	0.97	HMGCS1, HMGCR, MVK, MVD and LDLR, and further reduces the levels of intracellular fatty acid and cholesterol.
	0.94	HMGCS1, HMGCR, MVK, MVD and LDLR for cholesterogenesis, two chaperones, INSIG1 and SCAP.
	0.59	HMGCS1, HMGCR, MVK, MVD and LDLR and two chaperones, INSIG-1 and SCAP in LNCaP and C4-2B cells examined by qRT-PCR.
26153245	0.97	3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1); farnesyl-diphosphate farnesyltransferase 1 (FDFT1); squalene epoxidase (SQLE); methylsterol monooxygenase 1 (SC4MOL); cytochrome P450, family 51, subfamily A, polypeptide 1 (CYP51A1); stearoyl-CoA desaturase (SCD); fatty acid desaturase 1 (FADS1); low density lipoprotein receptor (LDLR); myosin regulatory light chain interacting protein (MYLIP); ATP-binding cassette, subfamily G, member 1 (ABCG1); and ATP-binding cassette, subfamily A, member 1 (ABCA1).
	0.94	LDLR, HMGCS1, FDFT1, SQLE, CYP51A1, SC4MOL, SCD, and FADS1), and 3 that were downregulated with increasing BMI (MYLIP, ABCG1, and ABCA1).
	0.80	LDLR, MYLIP), synthesis ( SCD, FADS1, HMGCS1, FDFT1, SQLE, CYP51A1, SC4MOL), and efflux ( ABCA1, ABCG1), producing a molecular profile expected to increase intracellular cholesterol.
26632252	0.97	HMGCS1, HMGCR, LDLR, ABCA1, ABCG1, ABCG5, ACACA, FASN and CYP27B1 after over-expression or depletion of hsa-miR-195 in MCF-7 cells using real time PCR analysis (Fig. 3B).
	0.94	HMGCS1, HMGCR), cellular uptake (LDLR) and cellular efflux (ATP-binding cassette transporters, ABCA1, ABCG1 and ABCG5).
30561264	0.97	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).
	0.87	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.
31685796	0.97	HMGCS1, human LDLR promoters and three Sterol regulatory elements (3SRE) with respect to reporter vector pGL3.0.
	0.87	HMGCS1 promoter, the human LDLR promoter, or three sterol regulatory elements (3SRE) that bind SREBP-2.
24829397	0.96	HMGCS1, LDLR, DHCR7), and cytokines (IL8, CCL20, CXCL1).
	0.94	HMGCS1, LDLR, DHCR7) and the YAP/Hippo pathway (CTGF, CYR61, SPARC) in addition to luminal/basal markers (KRT14, TP63), DKK1 (Wnt negative regulator), and PHLDA1, an important negative regulator and effector of Aurora A kinase in breast cancer.
	0.94	HMGCS1), 7-dehydrocholesterol reductase (DHCR7), and low-density lipoprotein receptor (LDLR) could result from either direct or indirect transcriptional regulation by ERBB4.
	0.88	LDLR, HMGCS1, and HMGCR were two of the top predicted activated transcription factors in the IPA analysis.
	0.78	LDLR, SPARC, HMGCR, HMGCS1, TP63, and KRT14, all of which were upregulated except for SPARC, which was reduced with ERBB4 expression (Figure 5B).
	0.74	HMGCS1, LDLR genes, which are chief regulators of the cholesterol pathway.
27308369	0.96	HMG-CoA synthase 1 (HMGCS1), and low-density lipoprotein receptor (LDLr) (Fig. 1B).
	0.89	HMGCS1, and LDLR, thereby blunting the anticancer efficacy of statins in tumor cells (3).
	0.85	HMGCS1, HMG-CoA synthase 1; SREBP2, sterol regulatory element binding transcription factor 2; FPP, farnesyl pyrophosphate; GGPP, geranaylgeranyl pyrophosphate; LDLr, low-density lipoprotein receptor.
30584280	0.96	HMGCS, and LDLR bands.
	0.92	HMGCS, 3-hydroxy-3-methylglutaryl-CoA synthase; LDLR, low-density lipoprotein receptor; NS, no significance; SREBP, sterol regulatory element-binding protein; WB, Western blotting.
19203388	0.96	HMGCS), the low density lipoprotein receptor (LDLR) and genes that control response to free radicals (HMOX1) and hypoxia (HIF1A) were significantly, but negatively, correlated with PER1 mRNA.
25788893	0.95	Ldlr, Hmgcr, Hmgcs1, and Insig1 expression was upregulated by DEHP, suggesting an increase in cholesterol sources.
28088440	0.95	low density lipoprotein receptor (LDLR), hydroxymethylglutaryl-CoA synthase (HMGCS)), and decrease cholesterol efflux (ATP-binding cassette, sub-family A, member 1 (ABCA1)), beta-oxidation (carnitine O-octanoyltransferase (CROT), trifunctional enzyme subunit beta (HADHB), and carnitine palmitoyltransferase 1A (CPT1A)), and SREBP inhibition (Sirtuin 6 (SIRT6), 5' AMP-activated protein kinase (AMPK), insulin receptor substrate 2 (IRS2)).
31497741	0.95	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).
32161285	0.95	LDLR, hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and HMGC synthase (HMGCS).
30237397	0.94	HMGCS1, HSD17B7, INSIG1, LSS, MSMO1, SQLE, LDLR, and ACAT2) (Fig. 6a), which is consistent with the mechanism of action of melittin.
	0.88	HMGCS1, HSD17B7, INSIG1, LSS, MSMO1, SQLE, LDLR, and ACAT2) in response to overexpression of NONHSAT105177; b Protein levels of cholesterol biosynthesis pathway molecule CLU in response to overexpression of NONHSAT105177. (*P < 0.05, **P < 0.01, ***P < 0.001)
28357032	0.94	HMGCS1, HMGCR, SQLE, CYP7A1 and LDLR.
24619155	0.93	HMGCS, and LDLR in NPC1 cells after incubation with HP-beta-CD (beta-CD: 10 mM) or HE-SS-PRX (beta-CD: 0.2 mM) for 24 h at 37 C. Data are normalized to the expression level of beta-actin.
	0.90	3-hydroxy-3-methylglutaryl-coenzyme A synthase (HMGCS), and low-density lipoprotein receptor (LDLR).
	0.90	HMGCS, and LDLR in NPC1 cells were evaluated after treatment with HE-SS-PRX or HP-beta-CD (Fig. 4B).
	0.66	HMGCS) and uptake (LDLR) machinery (Fig. 4B); therefore, HP-beta-CD treatment increases intracellular cholesterol level again through the uptake of LDL-derived cholesterols.
25563794	0.92	HMGCS, HMGCR, LDLR, farnesyl diphosphate synthase, and squalene synthase.
27071970	0.92	HMGCS1) and cholesterol uptake (LDLR, MYLIP, and PCSK9) were quantified (Figure 2A).
31711490	0.92	HMGCS1, SREBP) and uptake genes (LDLR) in three independent lines of patient fibroblasts (Fig. 3a, Additional file 1: Figure S2a, b).
23990020	0.91	HMGCS1 and LDLR in all the cell lines as compared with negative control (Supplementary Figures S3a and b).
	0.88	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.
24135873	0.90	3-hydroxy-3-methylglutaryl-coenzyme A synthase 1 (HMGCS) or low density lipoprotein receptor (LDLR), have been detected in human chondrocytes.
20338039	0.89	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).
22754327	0.89	low-density lipoprotein receptor (LDL-R), 3'-hydroxylmethyl glutaryl coenzyme A synthase (HMGCS) and 3'-hydroxylmethyl glutaryl coenzyme A reductase (HMGCR).
17052361	0.87	HMGCS1, HMGCR, FDPS, SC5DL and DHCR7; see legend to Fig. 1 for complete names), cholesterol transport (LDLR) and fatty acid biosynthesis (FASN and SCD1).
24246224	0.87	HMGCS1, LDLR, FADS1, FADS2).
18307821	0.83	LDLR and HMGCS1 is involved in lipid metabolism.
31102995	0.71	HMGCS1 (HMG-CoA synthase 1), FDFT1 (farnesyl-diphosphate farnesyltransferase 1), SQLE (squalene epoxidase), HMGCR, and LDLR (low-density lipoprotein receptor), were found to be recurrently regulated by many antipsychotics (Figure S6), supporting the lipid disturbance associated with antipsychotic medications.