Publication for Hmgcr and Fdps

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Hmgcr	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	15357			[link]
mmu	Fdps	farnesyl diphosphate synthetase	110196

Pubmed ID	Priority	Text
25918730	0.98	HMGR and FPPS are two key enzymes, locating upstream of mevalonate pathway, and directly or indirectly catalyze the synthesis of isoprenoid intermediates (FPP and GGPP).
	0.98	HMGR, FPPS, GGPPS, FNT, and GGT-1.
	0.96	HMGR and FPPS and similar SQS in the aorta from STZ-induced diabetic mice.
	0.96	HMGR inhibitors (statins) and FPPS inhibitors (nitrogen-containing bisphosphonate, N-BP) may inhibit the synthesis of isoprenoid intermediates, suppress the activation of small GTPase, attenuate the VSMC proliferation, and finally slow the progression of atherosclerosis induced by diabetes.
	0.96	HMGR and FPPS, the expressions of GGPPS, FNT, and GGT-1 were also remarkably upregulated in diabetic aortas.
	0.94	3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), farnesyl pyrophosphate synthase (FPPS), geranylgeranyl pyrophosphate synthase (GGPPS), farnesyltransferase (FNT), and geranylgeranyltransferase-1 (GGT-1), and unchanged expression of squalene synthase (SQS) and phosphor-3-hydroxy-3-methylglutaryl-coenzyme A reductase (P-HMGR) in 8 and 16 weeks of diabetes.
	0.80	HMGR, FPPS, GGPPS, FNT, and GGT-1 but did not change the expressions of SQS and P-HMGR.
	0.64	HMGR, FPPS, FNT-beta, GGT-1beta, squalene synthase (SQS), phosphor-3-hydroxy-3-methylglutaryl-coenzyme A reductase (P-HMGR), and geranylgeranyl pyrophosphate synthase (GGPPS) (Figure 1).
22441164	0.98	HMGCR, IDI1, FPPS, SQLE, and LSS was significantly decreased in WY-14,643-treated vs. control mouse liver (Fig. 4D).
	0.98	HMGCR, IDI1, FPPS, SQLE, LSS, SREBP-2) and ER stress markers (e.g., Grp78, TRIB3, ATF4, CHOP, p8) is already increased in livers from embryonic day 18.5 SW/129 Pex2-/- mice compared to controls (W.J. Kovacs and P.L. Faust, unpublished results).
	0.97	HMG-CoA reductase (HMGCR), IPP isomerase (IDI1), FPP synthase (FPPS) and squalene synthase (SQS), were normal in livers of newborn SW/129 strain Pex2-/- mice compared to age-matched controls, but all enzyme activities were significantly elevated in the postnatal knockout mouse livers.
	0.97	HMGCR, FPPS, IDI1, SQS, squalene epoxidase (SQLE), lanosterol synthase (LSS), 7-dehydrocholesterol reductase (DHCR7), LDL receptor (LDLR) and Insig-1 were all significantly increased 1.6- to 4.7-fold in P0 129 Pex2-/- versus control mouse liver.
	0.96	HMGCR protein levels were increased 3-fold, and IDI1 and FPPS protein levels were elevated 4-fold and 2.4-fold, respectively, in 129 Pex2-/- liver compared to controls (Fig. 1A).
	0.93	HMGCR, IDI1, and FPPS were decreased by ~40% (P=0.05) (supplemental Table S1), ~60% (P<0.001) (supplemental Table S2), and ~50% (P=0.06) (data not shown), respectively.
	0.66	HMGCR and SQS were already increased 2.1-fold, and IDI1 activity was increased 1.6-fold in the liver of P0 129 Pex2-/- mice, relative to controls; the activity of FPPS was similar in the liver of control and 129 Pex2-/- mice (cf.
21109190	0.98	HMGCR, farnesyl diphosphate synthase (FDPS) and squalene epoxidase (SQLE), as well as those of the cytoplasmic precursor form of SREBP-2 were decreased as assessed by Western blotting (Figure 1D).
	0.97	Hmgcr and Fdps (Figure S3A).
29710765	0.98	3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr) and farnesyl diphosphate synthase (Fdps), were expressed at similar or even lower levels in the livers of sedentary and of exercised control-fed mice (Figure 4B).
	0.97	Fdps and Hmgcr, which are key enzymes in cholesterol biosynthesis, to be upregulated by exercise.
19183246	0.98	FDPS, IDI1, NSDHL and SQLE are members of the mevalonate pathway downstream of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and represent potent therapeutic targets for cholesterol-lowering agents.
21631939	0.98	Hmgcr, Pmvk, Idi1, Fdps, and Lss, were all up-regulated between 1.3 to 3.0 fold at the transcript level.
22252456	0.98	Hmgcr, Pmvk, Mvd, Fdps, Nsdhl, Idi1, Sc4mol, Cyp51, and Dhcr7).
23260873	0.98	3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr), 7-Dehydrocholesterol reductase (Dhcr7), mevalonate kinase (Mvk), 3-hydroxy-3-methylglutaryl-coenzyme A synthase 1 (Hmgcs 1), farnesyl diphosphate synthase (Fdps) and squalene epoxidase (Sqle), were significantly down-regulated.
23533470	0.98	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), Farnesyl diphosphate synthase (FDPS), and Cytochrome P450, family 51 (CYP51) in the liver compared with HFD-fed mice.
23585733	0.98	Hmgcr, Sqle, Fdps, Idi1, and Ldlr) were all markedly down-regulated by 70%-90% (Figure 2E).
25794851	0.98	3-hydroxy-3-methylglutaryl-CoA reductase, farnesyl diphosphate synthetase, squalene synthase, and 3-hydroxy-3-methylglutaryl-CoA synthetase, which are all well-known downstream targets of Srebp-2 (Figure 8C).
26964834	0.98	3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), hydroxy-3-methylglutaryl-coenzyme A synthase 1 (HMGCS1), and farnesyl diphosphate synthase (FDPS).
27155921	0.98	farnesyl diphosphate synthase (Fdps), HMG-CoA reductase (Hmgcr), Cyp8b1, and farnesoid X receptor (Fxr) were significantly upregulated in PCB 126 exposed mice whereas mRNA levels of Cyp3a11 was decreased.
27878435	0.98	HMGCR, HSD3B7, HMGCS1, LSS, FDFT1, DHCR7, HSD17B7, NSDHL, DHCR24, FDPS, SIGMAR1, SQLE, MVK, that are expressed in the lens.
28725001	0.98	Hmgcr, farnesyl diphosphate synthetase (Fdps), and farnesyl diphosphate farnesyl transferase 1 (Fdft1), are transcriptionally regulated by sterol regulatory element-binding protein 2 (SREBP2) binding to sterol response elements (SREs).
29500098	0.98	HMG CoA reductase, farnesyl diphosphate synthase, squalene synthase, and the low-density lipoprotein (LDL) receptor.
30069000	0.98	Fdps, Hmgcr, Hmgcs1, Hsd17b7, Idi1, Lss, Mvd, Mvk, Msmo1, Nsdhl, Pmvk, Sc5d, Sqle, and Tm7sf2 were significantly decreased in HFD livers.
30619997	0.98	Hmgcr, including farnesyl diphosphate synthase (Fdps), squalene epoxidase (Sqle), and 7-dehydrocholesterol reductase (Dhcr7), were markedly elevated by approximately 2-fold to 3-fold in HMGCR KI livers compared to WT littermates (Fig. 3C) despite the absence of changes in the mRNA expression of the upstream activator sterol regulatory element binding transcription factor 2 (Srebf2) (Supporting Fig. S4C).
31540279	0.98	hmgcr, mvd, srebp2, and fdps, was significantly increased in H-RasV12-expressing NIH3T3 cells (Figure 4A).
26311497	0.97	HMGCR, HMGCS, LDLR, FDPS, SS, ACC, FAS, SCD-1 and GPAT, but also ameliorated gene expression in SREBP pathway, including SREBP-1a, SREBP-1c, SREBP-2 and Insig-1,without change in Scap expression (Fig. 6b).
	0.90	HMGCR, HMGCS, LDLR, FDPS (farnesyl diphosphate synthase), SS, FAS (FA synthase), SCD-1 (stearoyl CoA desaturase-1), ACC (acetyl CoA carboxylase), ACLY (ATP citrate lyase), GPAT (glycerol-3-phosphate acyltransferase), SREBP-1c, SREBP-2, and Insig-1 were all lower in PAQR3-shRNA group than in the control mice.
18852694	0.97	HMG-CoA reductase and farnesyl pyrophosphate synthase expression by fibrates was PPARalpha-dependent.
23957789	0.97	FDPS, HMGCR, and SC4MOL).
24324835	0.97	Hmgcr, Fdps, Fdft1, Acly, Fasn), and down regulates genes involved in lipoprotein secretion (ApoA4, ApoA5, Mttp), fatty acid uptake and elongation (Elovl3, Pnpla2), intracellular transport of cholesterol (Npc1), mitochondrial transfer of acyl CoA (Cpt2, Crot, Crat, Slc25a20) and beta oxidation (Acox1, Acox2, Acadm, Acadvl, Hadhb, Ech1, Acaa1) (Table S3).
25303682	0.97	3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr), farnesyl diphosphate synthase (Fdps), lanosterol synthase (Lss), 3-hydroxy-3-methylglutaryl-coenzyme synthase 1 (Hmgcs1), and sterol regulatory element-binding protein 2 (Srebp2) were significantly increased by ezetimibe.
26015368	0.97	3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase (HMGCR, the rate-limiting enzyme in cholesterol biosynthesis), HMG-CoA synthase (HMGCS), and farnesyl diphosphate synthase (FPPS) were all upregulated in GF mice.
26023080	0.97	3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr) and farnesyl diphosphate synthase (Fdps), were decreased by 44-98% in streptozotocin treated mice.
28150810	0.97	Hmgcr, Mvk, Fdps, Sqle, Lss, Nsdhl, Sc5d, and Dhcr24.
28244871	0.97	HMG-CoA reductase, farnesyl diphosphate synthase, squalene synthase, and PCSK9) were reduced by 60-80% in hepatocyte-Srebf-2-/- livers compared to controls.
28395113	0.97	HMGCR, farnesyl diphosphate synthase, squalene synthase, adenosine triphosphate-binding cassette transporter A 1 (a gene involved in cholesterol export26), and the gluconeogenic gene PEPCK in Ad-CRTC2 mouse livers (Fig. 5A).
29132502	0.97	HMGCS1, 3-hydrox-3-ymethylglutaryl-CoA reductase (HMGCR) and FDPS were either unaffected or increased in all knockouts (Figure 8D; Figure 8:figure supplement 1A), indicating that the mevalonate pathway is not impaired when mtDNA gene expression is disrupted.
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).
19589396	0.96	HMG-CoA reductase, farnesyl diphosphate synthase, squalene synthase, and lathosterol synthase in the liver are further investigated under the same experimental conditions as described above, it is observed that in control mice, expression levels of these SREBP-2-responsive genes are significantly reduced by the high cholesterol diet compared with the chow diet.
27394692	0.96	Fdps, and Hmgcr were down regulated in mice in OR and ORA diet groups compared to the OD diet group.
30321984	0.96	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), and farnesyl pyrophosphate synthase (FDPS), has been reported in a high fat diet-induced obese mice model.
25688136	0.95	Fdps, ggps1, Hmgcr, Hmgcs1, Hmgcs2) and coenzyme Q synthesis pathways (coq2, coq3, coq5, coq7, pdss1, pdss2) were not affected in Mfn2 knockout hearts (Fig. 5 C).
26232687	0.95	Hmgcr, Fdps, Sqs, and Lss, which are involved in cholesterol synthesis, were significantly higher in OVX ERalpha (+/+) mice than in OVX ERalpha (-/-) mice.
30483502	0.94	HMGCR), 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA), mevalonate kinase (MVK), phosphomevalonate kinase (PMVK), diphosphomevalonate decarboxylase (MVD), farnesyl diphosphate synthase (FDPS), farnesyl-diphosphate farnesyltransferase 1 (FDFT1), squalene epoxidase (SQLE), 7-dehydrocholesterol reductase (DHCR7), or related metabolites may be involved in modulating HSC biology.
22461453	0.91	Hmgcr, Mvd, Fdps, Sqle, and Dhcr7).
23139832	0.91	Hmgcr, Idi1, Fdps, Sqle, Dhcr7 and Pmvk), including Hmgcr - that is the gene encoding the rate limiting enzyme for cholesterol biosynthesis - were up-regulated at 4-wk..Upstream regulator analysis indicated that SREBF2, SREBF1, SIRT2, FOXO1, EGR2, PPARGC1B were predicted "active", whereas PPARA, CEBPE, HMGA1and WT1 were predicted "inhibit" (Table S5).
22962999	0.89	HMGCR, HMGCS, FDPS, and CYP51, which are involved in cholesterol synthesis, tended to increase in the fucoxanthin-fed mice compared with the control mice, although these differences were not statistically significant.
25593129	0.88	farnesyl diphosphate synthase (Fdps), HMG-CoA reductase (Hmgcr) and squalene synthase (Sqle), were unchanged (Fig. 3A).
25799309	0.87	Hmgcr, Sqle, Cnbp, Dhcr24, Nsdhl, Fdps, Sc4mol, Fdft1 and Tm7sf2), cholesterol transport and uptake (e.g., Cd36, Apoa4 and Ldlr), cholesterol homeostasis (e.g., Fabp4, Apoa4, Pcsk9 and Ldlr), triglyceride synthesis (Ces3, Ppap2a, Dgat2, Ppap2c and Pcsk9) and triacylglycerol catabolism (Lpl and Gk2) (Fig. 4A, Fig. 5E, F and S7-S8 Tables), indicating that the decreased expression of these hepatic genes involved in cholesterol and triglyceride metabolism might be responsible, or contribute to the decreased cholesterol and triglyceride levels observed in Rm155LG/Alb-Cre transgenic mice.
20054815	0.76	Hmgcr, Pmvk, and Fdps.
25849138	0.73	3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr), farnesyl diphosphate synthase (Fdps), squalene synthase (Fdft1), Cyp51 and the LDL receptor (Ldlr) were also normalized in LIRKO mice by treatment with FMO3 ASO (Fig. 2j).