Publication for Hmgcr and Lss

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression
CoexViewer
mmu Hmgcr 3-hydroxy-3-methylglutaryl-Coenzyme A reductase 15357 [link]
mmu Lss lanosterol synthase 16987

Pubmed ID Priority Text
25083875 0.98 3-hydroxy-3-methyl-glutaryl-CoA reductase (Hmgcr), and lanosterol synthase (Lss) were uniquely regulated by SIRT6, as the amplitude of circadian oscillation was enhanced in SIRT6 KO (Figure 2E).
0.98 Hmgcr, and Lss (Figure 2D).
0.88 Hmgcr, and Lss genes with increased circadian amplitude exclusively in SIRT6 KO versus WT.
0.72 Hmgcr and Lss promoters, is shown (Figures 5C and S8).
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increased in livers from embryonic day 18.5 SW/129 Pex2-/- mice compared to controls (W.J. Kovacs and P.L. Faust, unpublished results).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 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.
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) .
0.56 hmgcr, fdft1, sqle, and lss.
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).
23021221 0.98 Hmgcr, Lss and Dhcr24, were down-regulated by the HCHF diet, especially in LDLR KO mice (Figure 2B), with Dhcr24 being the most suppressed transcript among the entire set of transcripts evaluated.
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).
27878435 0.98 HMGCR, HSD3B7, HMGCS1, LSS, FDFT1, DHCR7, HSD17B7, NSDHL, DHCR24, FDPS, SIGMAR1, SQLE, MVK, that are expressed in the lens.
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.
27185526 0.97 Hmgcr (3-hydroxy-3-methylglutaryl-Coenzyme A reductase), and Lss (Lanosterol synthase), were also increased (Figure 5D).
28150810 0.97 Hmgcr, Mvk, Fdps, Sqle, Lss, Nsdhl, Sc5d, and Dhcr24.
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)).
30069000 0.97 Hmgcr, Hmgcs1, Hsd17b7, Idi1, Lss, Mvd, Mvk, Msmo1, Nsdhl, Pmvk, Sc5d, Sqle, and Tm7sf2 were significantly decreased in HFD livers.
25393872 0.73 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.



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