Publication for Dhcr7 and Hmgcr

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Dhcr7	7-dehydrocholesterol reductase	13360			[link]
mmu	Hmgcr	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	15357

Pubmed ID	Priority	Text
18677445	0.98	3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr; EC 2.3.3.10) and 7-dehydrocholesterol reductase (Dhcr7; EC 1.3.1.21).
	0.98	Dhcr7-dependent transcriptional changes show a high degree of overlap, and that NRIF reduction resulted in reduced expression of sterol-sensing domain protein SCAP, followed by a decrease in mRNA levels of SRE-motif containing genes (HMGCR, FASN, SREBP2, S1P, and SQS1).
	0.98	Hmgcr and Dhcr7 were down regulated in NRIF-shRNA expressing Neuro2a cells (-DeltaDeltaCt=-0.48, p<0.01 and -DeltaDeltaCt= -0.68, p<0.01, respectively) (Fig. 3), suggesting that NRIF is involved in regulation of cholesterogenic transcripts.
	0.98	Hmgcr were regulated by NRIF, and NRIF-dependent and Dhcr7-dependent cholesterol biosynthesis transcripts significantly overlapped, we further hypothesized that NRIF is critical for the regulation of cholesterol-dependent transcripts.
	0.98	Hmgcr and Dhcr7, the first and last enzymes in cholesterol biosynthesis pathway.
	0.97	Hmgcr and Dhcr7 transcripts were significantly down regulated (-DeltaDeltaCt=-0.48, p<0.01 and -DeltaDeltaCt=-0.68, p<0.01, respectively)
	0.96	Hmgcr and Dhcr7, the first and last enzymes in the cholesterol biosynthesis pathway, we hypothesized that this regulation is mediated through NRIF.
	0.96	Hmgcr and Dhcr7 in Neuro2a neuroblastoma cell line; (2) Dhcr7 and NRIF down regulation have similar consequences on the expression of several signaling genes; (3) NRIF silencing itself leads to reduced expression of genes involved in sterol-regulated biosynthesis; (4) NRIF-dependent transcriptional regulation is present both in the absence and presence of exogenous cholesterol, suggesting that preservation of endogenous control over cholesterol biosynthesis in neurons cannot be replaced by exogenous sources; and (5) the regulatory role of NRIF on gene transcription is conserved across in vitro and in vivo experimental systems (Neuro2a and NRIF KO mice, respectively).
	0.94	Hmgcr and Dhcr7, two critical enzymes of the cholesterol biosynthesis pathway, (2) NRIF- and Dhcr7-dependent transcript changes will overlap, (3) NRIF reduction will affect the expression of genes that contain sterol-regulatory element sequences, and (4) the most critical changes in the expression of cholesterol biosynthesis genes produced by absence of NRIF will be present under both in vitro and in vivo conditions.
	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
18951487	0.98	Dhcr7 and Hmgcr, respectively) of the cholesterol biosynthesis pathway (Fig. 1).
	0.98	Hmgcr and Dhcr7 are highly expressed in Neuro2a cells.
	0.98	Hmgcr and Dhcr7, the first and the last enzymes in the cholesterol biosynthesis pathway, are highly expressed in Neuro2a neuroblastoma cells.
22394543	0.98	Hmgcr as well as Srebp-2, Cyp51 and Dhcr7 were significantly upregulated in mice on the Western diet when compared to the control group.
	0.97	Hmgcr, Cyp51 and Dhcr7 in liver samples of the mice fed the Western diet, suggesting that hepatic cholesterol synthesis is increased as well.
31676775	0.98	Hmgcr was modest at the gene and protein level at the time of sacrifice, several other key genes, including Dhcr7, Sqle, and Cyp51, suggest that, overall, TCDD exposure is repressing cholesterol biosynthesis in mice of both sexes.
	0.96	Hmgcr, such as 7-dehydrocholesterol reductase (Dhcr7), squalene epoxidase (Sqle), and Cytochrome P450, family 51 (Cyp51) (Table 1).
19183246	0.98	DHCR7, DHCR24, 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.
20054815	0.98	Hmgcr and Dhcr7, the rate-limiting and final enzymes in cholesterol biosynthesis, respectively, within cortical, hippocampal, and basal forebrain-cholinergic neurons.
22252456	0.98	Hmgcr, Pmvk, Mvd, Fdps, Nsdhl, Idi1, Sc4mol, Cyp51, and Dhcr7).
22441164	0.98	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.
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.
23512606	0.98	HMGCR, 7-dehydrocholesterol reductase (DHCR7) and squaleneepoxidase (SQLE) were downregulated in mice treated with miR-122 inhibitors.
24958265	0.98	3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr) and 7-dehydrocholesterol reductase (Dhcr7).
26315393	0.98	HMGCR, HMGCS1, DHCR7, LDLR, ABCA1, and INSIG1.
27878435	0.98	HMGCR, HSD3B7, HMGCS1, LSS, FDFT1, DHCR7, HSD17B7, NSDHL, DHCR24, FDPS, SIGMAR1, SQLE, MVK, that are expressed in the lens.
27900259	0.98	Hmgcr, Dhcr7, and Ldlr in GF compared to SPF mice, suggesting a reinforced endogenous biosynthesis and sensitivity towards hepatic uptake of cholesterol (Figure 6).
30069000	0.98	Dhcr7, Fdft1, Fdps, Hmgcr, Hmgcs1, Hsd17b7, Idi1, Lss, Mvd, Mvk, Msmo1, Nsdhl, Pmvk, Sc5d, Sqle, and Tm7sf2 were significantly decreased in HFD livers.
30463396	0.98	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), stearoyl-CoA desaturase (SCD), cytochrome P450 family 51 subfamily A polypeptide 1 (CYP51A1), acyl-CoA synthetase short-chain family member 2 (ACSS2), and 7-dehydrocholesterol reductase (DHCR7).
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).
30735525	0.98	HMG-CoA reductase (Hmgcr), mevalonate diphospho decarboxylase (Mvd), cytochrome P450 family 511 (Cyp51), 7-dehydrocholesterol reductase (Dhcr7), and cholestenol delta-isomerase (Ebp) were remarkably decreased by treatment with PD153035 (Fig 4C).
25556834	0.97	HMGCR gene expression is mild in N171-82Q mice (transgene expressed from prion promoter) reduced expression of HMGCR, HMGCS1, DHCR7, and CYP51 are observed in HD human and other mouse models.
	0.96	HMGCR levels, and also increased expression sterol biosynthesic enzymes: HMG-CoA synthase 1 (HMGCS1), lanosterol 14alpha-demethylase (CYP51), and 7-dehydrocholesterol reductase (DHCR7) (Figures 3C-F; Figures S3 C-F).
21724437	0.97	HMGCoA reductase protein in fibroblasts isolated from the Dhcr7 knockout mouse mediated by an apparent action of 7-DHC on the ER membrane.
22436747	0.97	3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr), 3-hydroxy-3-methylglutaryl-coenzyme A synthase 1 (Hmgcs1), and 7-dehydrocholesterol reductase (Dhcr7).
28282965	0.97	Dhcr7, Hmgcr, Ldlr) and mitochondria (FDR < 7e-7, e.g. Atp5e, Cox5a, Mrps24), among other processes.
28720595	0.97	Hmgcr, Sqle, Scd5, Hsd17b7 and Dhcr7, are upregulated.
31296899	0.97	Hmgcr, Mvd, Hsd17b7, and Dhcr7) and steroid hormone synthesis (StAR, StARD3, and Hsd17b7), but downregulation of the genes driving TG synthesis from the lists of GSEA (Fig. 3E, Supplementary Fig. 5).
27394692	0.96	Dhcr7, Fdps, and Hmgcr were down regulated in mice in OR and ORA diet groups compared to the OD diet group.
27097157	0.95	DHCR7 and HMGCR, respectively, in the cholesterol biosynthetic pathway.
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.
19631568	0.93	HMGCR activity results in early embryonic lethality around the time of implantation, while mutants lacking 7-dehyrocholesterol reductase (DHCR7), the last enzyme of the pathway, die within the first days after birth.
23139832	0.90	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).
22461453	0.89	Hmgcr, Mvd, Fdps, Sqle, and Dhcr7).
23299886	0.87	Hmgcr, Mvk, Pmvk, Dhcr7, Erg1, Fdft1 and Mvd is not seen in the Xbp1 liver knockout.