Publication for Hmgcr and Sqle
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Hmgcr | 3-hydroxy-3-methylglutaryl-Coenzyme A reductase | 15357 | [link] | ||
| mmu | Sqle | squalene epoxidase | 20775 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 23892605 | 0.98 | HMG CoA reductase (HMGCR) and SQLE. |
| 0.98 | HMGCR upstream of SQLE that is essential for learning and synaptic plasticity, and is important for the interaction between neurons and astrocytes at the synapse. | |
| 0.97 | HMGCR and SQLE. | |
| 0.97 | Hmgcr, Sqle and Cyp46a1 were downregulated in both alleles (Fig. 4b). | |
| 0.95 | Sqle or Hmgcr expression, though 129.Mecp2tm1.1Bird/Y mice have increased expression of both genes, regardless of SqleSum3Jus mutation status (Fig. 3e). | |
| 0.94 | Sqle expression was reduced by nearly 50% in SqleSum3Jus/+ brains at P70, with no compensatory change in Hmgcr (Fig. 3d; Supplementary Table 2). | |
| 0.93 | Hmgcr and Sqle were predictive of the behavior of genes encoding intermediate enzymes in the pathways (data not shown). | |
| 0.84 | Hmgcr and Sqle was unchanged in P28 and significantly higher in P56 129.Mecp2tm1.1Bird/Y livers compared to wild type (p<=.05; Fig. 4e). | |
| 0.79 | Hmgcr and Sqle in Mecp2tm1.1Bird/Y and Mecp2tm1.1Jae/Y differ in liver. | |
| 0.71 | Sqle but not Hmgcr is decreased in SqleSum3/+ brain; e) gene expression is unchanged by SqleSum3/+ in liver. | |
| 0.53 | Hmgcr, Sqle and Cyp46a1 in Mecp2tm1.1Bird/Y and Mecp2tm1.1Jae/Y are similar in brain. | |
| 19691840 | 0.98 | Hmgcr, Sqle, Lss, and Sc5d) were up-regulated (Table 2 and 3); however, the ratio of lathosterol to cholesterol did not confirm increased cholesterol biosynthesis (Figure 1B, pale grey boxes). |
| 0.94 | Hmgcr, Insig1 and Sqle while expression of Cyp51a1 and Srebp2 remained unchanged. | |
| 0.78 | HMG-CoA reductase (Hmgcr) and squalene epoxidase (Sqle), mechanisms other than direct transcriptional activation by CAR have to be considered. | |
| 0.72 | Hmgcr, Sqle and Insig1 promoters was performed to search for potential CAR binding sites. | |
| 0.56 | Hmgcr, Sqle promoters. | |
| 30954949 | 0.98 | Hmgcr, Sqle, Mvd and Elovl6 were homogeneously upregulated, whereas Fasn expression was strongly downregulated, in Fasn(-) HCCs (online supplementary figure S8). |
| 0.98 | Hmgcr, Sqle and Mvd (figure 2D), resulting in highest CE levels in Fasn(-) HCC (figures 2D and 4D). | |
| 0.94 | Hmgcr, squalene monooxygenase (Sqle) (padj=0.057), diphosphomevalonate decarboxylase (Mvd), which are involved in the mevalonate and cholesterol biosynthesis pathways, were highest in Fasn(-) HCCs and cytochrome P450 family 7 subfamily a member 1 (Cyp7a1) (padj=0.205) and cytochrome P450 family 7 subfamily b member 1 (Cyp7b1), two key enzymes responsible for cholesterol ester (CE) degradation, were lowest in the same tumours (figure 2B and D). | |
| 0.73 | Hmgcr, Mvd and Sqle in Fasn(+) and Fasn(-) HCCs from PIK3CA/c-Met and PIK3CA/Ras mice. | |
| 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. |
| 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). | |
| 27288453 | 0.98 | HMG-CoA reductase (Hmgcr), squalene epoxidase (Sqle) and lanosterol synthase (Lss), enzymes of the cholesterol biosynthesis pathway, were all increased ~3-fold in 129.Mecp2/Y liver by 8 weeks of age (Fig. 1C-E). |
| 0.98 | Hmgcr and Sqle, as well as rate-limiting enzymes of the triglyceride synthesis pathway Scd1 and Fasn (Fig. 5C). | |
| 0.94 | HMG-CoA reductase inhibitors (statins) phenocopies symptom improvement by Sqle mutation. | |
| 21762780 | 0.98 | HMG-CoA reductase and squalene monooxygenase enzyme levels were decreased by half in POR-null mouse livers, which we attributed to secondary post-translational down-regulation of these enzymes in response to elevated levels of 24-dihydrolanosterol; lanosterol and 24-dihydrolanosterol have been shown to enhance the degradation of HMG-CoA reductase but not squalene monooxygenase. |
| 0.94 | HMG-CoA reductase and squalene monooxygenase, 7-dehydrocholesterol reductase protein levels were increased several-fold in POR-null mouse liver in the present study (Fig. 1), consistent with the modest increase seen in mRNA level for this enzyme. | |
| 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) . |
| 0.50 | hmgcr, fdft1, sqle, and lss. | |
| 23585733 | 0.98 | Hmgcr, Sqle, Fdps, Idi1, and Ldlr) were all markedly down-regulated by 70%-90% (Figure 2E). |
| 0.98 | Hmgcr, Sqle, Idi1, and Ldlr) by 10%-27% in the cerebral cortex and hypothalamus, as well as some decrease in Srebf2 mRNA (Figure 3E). | |
| 24723866 | 0.98 | Hmgcr, Sqle and Cyp46a1) which encode key enzymes (3-hydroxy-3-methylglutaryl-CoA reductase, squalene epoxidase, CYP46A1) in the cholesterol metabolic pathway and cholesterol concentrations are altered in the brain in a development dependent manner (Buchovecky et al.,). |
| 0.97 | HMGCR and SQLE as the rate-limiting enzymes. | |
| 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. |
| 0.97 | Hmgcr, Mvk, Fdps, Sqle, Lss, Nsdhl, Sc5d, and Dhcr24. | |
| 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). | |
| 32111832 | 0.98 | 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) and squalene epoxidase (SQLE), and the low-density lipoprotein receptor (LDLR). |
| 0.97 | HMGCR, LDLR, SQLE, and FASN in response to sterol-depletion, in Hap1-SPRINGKO cells basal expression of these genes was reduced and the response to sterol-depletion was largely abrogated. | |
| 19183246 | 0.98 | 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. |
| 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). |
| 22855714 | 0.98 | Hmgcr, Fdft1, Dhcr24, Sqle and Idi1) and in the uptake of extracellular cholesterol (Ldlr) (Fig. 5B). |
| 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. |
| 23299886 | 0.98 | Hmgcr, Mvk, Pmvk, Mvd, Fdft1 and Sqle/Erg1 in the cholesterol biosynthetic pathway are decreased in SRSF3HKO liver. |
| 23812589 | 0.98 | 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), squalene epoxidase (SQLE) and isopentenyl-diphosphate delta isomerase 1 (IDI-1), which were verified by real-time PCR analysis (Fig. 3d). |
| 24025456 | 0.98 | SQLE has been proposed as the second rate-limiting enzyme in cholesterol synthesis since addition of cholesterol suppressed Sqle and Hmgcr mRNAs to the same extent. |
| 25739789 | 0.98 | Hmgcr, Sqle, Dhcr24, Tm7sf2), together with Srebf2 (Fig. 3a). |
| 26982734 | 0.98 | Hmgcr, Hmgcs, Fasn, Acaca and Sqle, were upregulated in activated CD8+ T cells. |
| 27255552 | 0.98 | Hmgcr, Pmvk, Sqle and Sc4mol) which target SREBP; a major transcriptional regulator of cholesterol metabolism. |
| 27424223 | 0.98 | Hmgcr, Hmgcs and Sqle) and fatty acid synthesis (Acaca and Fasn). |
| 27878435 | 0.98 | HMGCR, HSD3B7, HMGCS1, LSS, FDFT1, DHCR7, HSD17B7, NSDHL, DHCR24, FDPS, SIGMAR1, SQLE, MVK, that are expressed in the lens. |
| 29406859 | 0.98 | hmgcr, cyp51, sqle, mvd, and dhcr24 (Online Figures 6C and 6D). |
| 29965978 | 0.98 | Hmgcr and Sqle are increased in the skin of chow-fed SKO mice. |
| 30069000 | 0.98 | 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). |
| 31327168 | 0.98 | Hmgcr, Acss2, Pmvk, Mvd, Fdft1, Ldlr, and Sqle (Figure 2A). |
| 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. | |
| 28720595 | 0.97 | Hmgcr, Sqle, Scd5, Hsd17b7 and Dhcr7, are upregulated. |
| 0.81 | HMGCR), squalene epoxidase (SQLE) and various post-lanosterol reductase and dehydrogenase steps. | |
| 20045742 | 0.97 | 3-hydroxy-3-methylglutaryl-Coenzyme A reductase and squalene epoxidase) and phospholipids (i.e. CTalpha and PSS1), as well as lipoprotein turnover (i.e. LDLr and ABCA1). |
| 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). |
| 22302795 | 0.97 | HMG CoA-reductase (Hmgcr) and Squalene epoxidase (Sqle), Connexin 32 (Cx32), and Peripheral Myelin Protein 22 (Pmp22) in mutant animals by quantitative RT-PCR, and found that they were strongly downregulated relative to wild type (Fig. 5E) at multiple developmental timepoints. |
| 25506514 | 0.97 | HMGCR and SQLE. |
| 27683878 | 0.97 | Hmgcr, Sqle, and Lss are not altered in Zfp191null OPCs and oligodendrocytes, suggesting a more complex level of regulation. |
| 30008738 | 0.97 | HMG-CoA reductase (Hmgcr), squalene epoxidase (Sqle), mevalonate (diphospho) decarboxylase (Mvd), and lanosterol synthase (Lss), were remarkably decreased in the HL group compared to the HU group (Figure 4(c)). |
| 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). |
| 31284522 | 0.97 | Hmgcr and Squalene Epoxidase (Sqle), in both brains and livers of Mecp2-null mice and a concurrent reduction of cholesterol precursors and a decrease of cholesterol biosynthesis in the brain. |
| 27502578 | 0.96 | Hmgcr and Sqle (Fig. 2E,F). |
| 20303728 | 0.95 | squalene epoxidase (Sqle), NAD(P)-dependent steroid dehydrogenase-like (Nsdhl), 3-hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr), were also decreased in the HFLD-fed mice. |
| 27309819 | 0.95 | HMGCR and SQLE that decreased in abundance. |
| 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. |
| 31974378 | 0.92 | Hmgcr, and Sqle (Fig. 1g), but showed no influence on genes controlling cholesterol efflux or uptake, including Abca1, Abcg1, Ldlr, and Ldol (Supplementary Fig. 7). |
| 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). |
| 23563690 | 0.91 | Hmgcr, Hmgcs, Sqle) and fatty acid biosynthesis genes (Acaca, Fasn) (Fig. 1a), and the addition of CD28 costimulation did not provide additional induction of the program. |
| 32027669 | 0.90 | Hmgcr, Sqle) and fatty acids (Fasn, Scd1), but also direct cholesterol transport (Ldlr, Pcsk9, Stard4) and retinoid synthesis (Aldh1a1, Rdh11). |
| 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. |
| 28874658 | 0.87 | HMGCR and SQLE. |
| 27355629 | 0.80 | 3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr) and squalene epoxidase (Sqle) are in the list of the most significantly downregulated genes in this analysis (Table 2). |
| 21044070 | 0.69 | HMG CoA Reductase, HMG CoA Synthase, Lanosterol Demethylase, Squalene Epoxidase, and Stearoyl CoA Desaturase:by quantitative PCR analysis of independent ChIP assays (Figure S2). |
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