Publication for Fdft1 and Hmgcr

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Fdft1	farnesyl diphosphate farnesyl transferase 1	14137			[link]
mmu	Hmgcr	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	15357

Pubmed ID	Priority	Text
31767163	0.98	HMG-CoA reductase (HMGCR; Figure 5A) and squalene synthase (FDFT1; Figure 5B), were decreased already after 24 h from the onset of differentiation [one-way ANOVA; HMGCR: F (3,16) = 79.51; p < 0.0001; FDFT1: F (3,16) = 29.06; p < 0.0001, respectively].
	0.95	HMG-CoA reductase and squalene synthase enzymes, as well as of LDLR and LRP1 (HMGCR: t(4) = 9.38, p = 0.007; FDFT1: t(4) = 17.43, p < 0.0001; LDLR: t(4) = 11.80, p = 0.0003; LRP1; t(4) = 0.60, p = 0.58).
	0.94	HMGCR and FDFT1, albeit to a smaller extent.
22234961	0.98	3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), farnesyl-diphosphate farnesyltransferase (FDFT1), squalene epoxidase (SE) and oxidosqualene cyclase (OSC), all of which have been shown to be under the regulation of the transcription factor sterol element binding protein 2 (SREBP2) .
	0.54	hmgcr, fdft1, sqle, and lss.
23299886	0.98	Hmgcr, Mvk, Pmvk, Mvd, Fdft1 and Sqle/Erg1 in the cholesterol biosynthetic pathway are decreased in SRSF3HKO liver.
	0.86	Hmgcr, Mvk, Pmvk, Dhcr7, Erg1, Fdft1 and Mvd is not seen in the Xbp1 liver knockout.
26049045	0.98	HMG-CoA reductase and squalene synthase, were more abundant in the livers of KO than of WT mice, as was the mRNA for sterol regulatory element-binding protein-2 (SREBP-2), a transcription factor that up-regulates the transcription of genes encoding several enzymes involved in cholesterol synthesis (Table 1).
	0.98	HMG-CoA reductase, which catalyzes the rate-limiting step in cholesterol biosynthesis, squalene synthase, which catalyzes the first step in the pathway that produces cholesterol from farnesyl pyrophosphate, and the transcription factor SREBP-2 is a normal response to low plasma cholesterol.
30069000	0.98	Fdft1, Fdps, Hmgcr, Hmgcs1, Hsd17b7, Idi1, Lss, Mvd, Mvk, Msmo1, Nsdhl, Pmvk, Sc5d, Sqle, and Tm7sf2 were significantly decreased in HFD livers.
	0.98	Fdft1, Hmgcs, Hmgcr.
19183246	0.98	FDFT1, 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.
20435134	0.98	Hmgcr, Fdft1, and Soat1) and transcription factors (Srebf1, CNBP and Hbp1) involved in cholesterol biosynthesis were all significantly up-regulated in APP23 brain in late disease stages (Supplementary Table 6, APP23LATE), indicating the existence of a causative relationship between APP and cholesterol production.
22400114	0.98	HMG-CoA reductase, squalene synthase, acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS).
22855714	0.98	Hmgcr, Fdft1, Dhcr24, Sqle and Idi1) and in the uptake of extracellular cholesterol (Ldlr) (Fig. 5B).
23347841	0.98	squalene synthase, HMG-CoA synthase, HMG-CoA reductase, and SREBP2) was downregulated by 25-HC.
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).
26311497	0.98	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), HMGC synthase (HMGCS), LDL receptor (LDLR) and squalene synthase (SS) (Fig. 1c).
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.
30037080	0.98	3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA-r), squalene synthase, and ABCG8, suggesting that dietary cholesterol could promote fatty liver disease by modulating expression of these genes.
31327168	0.98	Hmgcr, Acss2, Pmvk, Mvd, Fdft1, Ldlr, and Sqle (Figure 2A).
32111832	0.98	Hmgcr, Sqs, Dhcr24, Pcsk9, and Ldlr (Fig. 4c).
22441164	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.
	0.69	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.
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).
	0.97	HMGCR, HMGCS, squalene synthase, and LDLR) and other lipid transport genes (adenosine triphosphate-binding cassette transporter A 1 and ACAT2) was reduced in CRTC2-/- mice (Fig. 5D).
28459857	0.97	Hmgcr, Fdft1, Sqle and Ldlr, while the expression of ApoE was reduced by more than six-fold (data not shown).
	0.97	Hmgcr, Fdft1 and Sqle) was observed.
21203578	0.97	HMG-CoA reducatase (Hmgcr) and numerous genes in this pathway such as mevalonate kinase (Mvk), squalene epoxidase (Sqle), isopentenyl-diphosphate delta isomerase 1 (Idi1), and farnesyl diphosphate farnesyl transferase 1 (Fdft1).
23838163	0.97	HMG-CoA reductase, HMG-CoA synthase, squalene synthase, and LDLR was higher with OS than PS (Figure 1C).
23957789	0.97	FDFT1, 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).
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.
29262627	0.97	squalene synthase (SQS), and the 3-Hydroxy-3-methylglutaryl-CoA reductase (HMGCR), among others significantly drive the tumorigenic process and increases the aggressiveness of the tumors.
30334382	0.97	HMGCR and upregulations of cholesterol synthesis enzymes mevalonate kinase (Mvk), phosphomevalonate kinase (Pmvk), farnesyl-diphosphate farnesyltransferase 1 (Fdft1/Sqs), and squalene epoxidase (Sqle).
20633110	0.96	HMG-CoA reductase pathway is a study which reported that cells treated with the squalene synthase inhibitor, zaragozic acid, showed over a 250-fold increase in FPP levels but only a 4-fold increase in GGPP levels in the mouse fibroblast cell line NIH3T3.
25918730	0.95	HMGR and FPPS and similar SQS in the aorta from STZ-induced diabetic mice.
	0.93	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.
	0.72	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).
19589396	0.95	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.
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.
27313533	0.95	HMGCR, and FDFT1 in HSC activation and MFB function.
28874658	0.95	Hmgcr, Sqs and Hmgcs1 transcripts in prostate of wild type (WT) and Pten pc -/- mice.
30483502	0.95	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.
28808191	0.94	HMGCR and squalene synthase (also called farnesyl diphosphate farnesyltransferase)[ , - ].
21451815	0.93	Hmgcr, Idi2 and Fdft1 sites that regulate cholesterol homeostasis.
25593129	0.92	HMG-CoA reductase (Hmgcr) and squalene synthase (Sqle), were unchanged (Fig. 3A).
19117526	0.87	Hmgcr or squalene synthase result in early embryonic lethality in mouse models.
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.
25849138	0.70	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).