Publication for Cyp51 and Hmgcr

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Cyp51	cytochrome P450, family 51	13121			[link]
mmu	Hmgcr	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	15357

Pubmed ID	Priority	Text
29237705	0.98	Hmgcr, Idi1, and Cyp51), as well as the known target gene Axin, were found to be up-regulated (Fig. 5 A).
	0.98	Hmgcr, Idi1, and Cyp51 (Fig. S3 D), whereas knocking down the expression of beta-catenin inhibited the expression of these enzymes (Fig. 5 B).
	0.98	HMGCR, IDI1, CYP51, and mouse Hmgcr (Fig. 5 C), suggesting that beta-catenin signaling directly regulates Hmgcs1, Hmgcr, Idi1, and Cyp51 transcription.
	0.97	Hmgcr, Cyp51, and Idi1 after disrupted ciliogenesis.
	0.97	Hmgcr, Idi1, and Cyp51, and overexpression of beta-catenin significantly activated these promoters in luciferase assays (Fig. S3 E).
28962244	0.98	Cyp51 (1.7-fold) and HMG-CoA red (1.9-fold) (Fig. 2B).
	0.97	Cyp51 (1.4-fold), HMG-CoA red (1.6-fold), and Por (1.4-fold) in comparison with vehicle-treated cells (Fig. 2B).
	0.85	cytochrome P450 enzyme 51 (Cyp51), HMG-CoA reductase (HMG-CoA red), and cytochrome P450 oxidoreductase (Por).
24391516	0.98	HMG-CoA reductase (HMGR), as well as the expression of the lanosterol 14 -demethylase, Cyp51, both essential enzymes in cholesterol biosynthesis and intermediate metabolites.
	0.98	HMGR our analysis identified circadian cycles of protein abundance in the mouse liver for several key enzymes involved in cholesterol and bile acid synthesis such as HMG-CoA synthase 1 (HMGCS1), isopentenyl-diphosphate delta-isomerase 1 (IDI1), CYP51, CYP7A1 and CYP8B1 (Figure 6 and S4F).
24465397	0.98	HMG-CoA reductase and CYP51 as well as enzymes responsible for fatty acid synthesis such as SCD1 and 2 were significantly increased in the jejunum of ISR2 mice.
	0.96	HMG-CoA reductase and CYP51 enzymes involved in cholesterol synthesis was increased as well as the expression of SCD1 and SCD2 enzymes involved in fatty acid synthesis.
30069000	0.98	Cyp51, Dhcr7, Fdft1, Fdps, Hmgcr, Hmgcs1, Hsd17b7, Idi1, Lss, Mvd, Mvk, Msmo1, Nsdhl, Pmvk, Sc5d, Sqle, and Tm7sf2 were significantly decreased in HFD livers.
	0.98	Cyp51, Fdft1, Hmgcs, Hmgcr.
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	CYP51, 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.
22252456	0.98	Hmgcr, Pmvk, Mvd, Fdps, Nsdhl, Idi1, Sc4mol, Cyp51, and Dhcr7).
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.
25697398	0.98	hmgcr and cyp51 gene are all significantly increased in stress-responsive animals after FSS (Fig. 2A), and the expression levels of genes mediating neuronal uptake of cholesterol, such as ldlr and lrp1, or astroglial exportation of cholesterol, such as abca1 and abcg1, are also increased (Fig. 2B and D).
26938273	0.98	Hmgcr, Mvd, Cyp51a1, and Srebf2), which were reported to facilitate structural remodeling of the small intestine, in the upper part of the small intestine (Fig 6C) but not in the lower part (Fig 6D).
27334049	0.98	lanosterol 14alpha-demethylase in Crem-/- mice, lanosterol accumulates in the testes and can lead to an increase in HMGCR degradation.
27878435	0.98	CYP51A1-PPI network reveals an enrichment for sterol biosynthetic process (GO:0016126) categories that includes 15 protein-protein interaction candidates, namely, TM7SF2, MVD, HMGCR, HSD3B7, HMGCS1, LSS, FDFT1, DHCR7, HSD17B7, NSDHL, DHCR24, FDPS, SIGMAR1, SQLE, MVK, that are expressed in the lens.
28150810	0.98	Hmgcr, Idi1, Sqle, Cyp51, Msmo1, Hsd17b7, and Dhcr24) were among the genes down-regulated in XX/Sry Sertoli cells, suggesting that the down-regulation of the cholesterogenic genes was primarily the result of the decreased expression of Srebf2.
29406859	0.98	hmgcr, cyp51, sqle, mvd, and dhcr24 (Online Figures 6C and 6D).
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).
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).
22394543	0.97	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.
25556834	0.97	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).
	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.
28459857	0.97	Hmgcr, Cyp51 and others in the steroid biosynthetic pathway), but an increase in the transcription of the Soat1 and Soat2 enzymes which catalyze Chl esterification to Chl-palmitate, as well as of Abcg5, pointing to an increased Chl ester efflux from the brain.
29899496	0.97	Cyp51, Srebf1, Sp1), sterol synthesis and metabolism genes (Hmgcr, Hmgcs1, Cyp27a1, Ch25h), and sterol trafficking genes (Lrp1, Vldlr, Osbp) in 15-week HF/HC-fed female mice WAT (Fig. 5a and Supplementary Fig. S3a).
27977712	0.96	Cyp51; fold change, 5.6), 3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr; fold change, 2.5), hydroxysteroid (17-beta) dehydrogenase 7 (Hsd17b7; fold change, 2.8), insulin induced gene 1 (Insig1; fold change, 1.8), sterol-C4-methyl oxidase-like (Sc4mol; fold change, 4.5), and leptin receptor (Lepr; fold change, 1.6) were upregulated.
	0.79	Cyp51, Hmgcr, and Insig1) and fatty acid beta-oxidation (Acsl3), whereas it significantly downregulated expression of genes related to fatty acid biosynthesis (Scd1, Acot11, and Mlxipl/carbohydrate responsive element-binding protein [ChREBP]), triacylglycerol biosynthesis (Mogat1), oxidative stress (growth differentiation factor 15, Gdf15), inflammatory and immune processes (Cfd, Chi3l1, Ctse, Orm2, Rorc, and Tlr5), ceramide biosynthesis (Sptlc3), and lipid storage (Plin4).
28420650	0.96	3-hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr), and lanosterol 14alpha-demethylase (Cyp51)] in the liver (Fig. 4C).
19691840	0.94	Hmgcr, Insig1 and Sqle while expression of Cyp51a1 and Srebp2 remained unchanged.
24065951	0.93	Cyp51 was abolished, while the expression of Hmgcr remained circadian.
25593129	0.92	cytochrome P450 51 (Cyp51), farnesyl diphosphate synthase (Fdps), HMG-CoA reductase (Hmgcr) and squalene synthase (Sqle), were unchanged (Fig. 3A).
22962999	0.91	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.
28098217	0.77	Hmgcr-/- mice survive for up to 5 weeks, while mice lacking the rate limiting step of the post-lanosterol pathway, the hepatocyte Cyp51-/- mice, survive for over 19 weeks although with marked changes in liver structure and function.
25849138	0.76	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).
25393872	0.72	Hmgcr, Lss and Ebp from cholesterol synthesis (Table S5), which is in line with Gatti et al and relates well with Lorbek et al. However, in our study we investigated sexual dimorphism in context of Cyp51 genotype and we uncovered novel differences at the level of expression of cholesterogenic genes.
27535584	0.72	Cyp51, Cyp7a1, Cyp8b, Por, Hmgcr) and regulators of metabolism (Ppara, Ppargc1a, Car, Rxr).