Publication for Hmgcr and Dhcr24
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Hmgcr | 3-hydroxy-3-methylglutaryl-Coenzyme A reductase | 15357 | [link] | ||
| mmu | Dhcr24 | 24-dehydrocholesterol reductase | 74754 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 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. |
| 0.98 | Dhcr24 and Hmgcr were both down-regulated at between 1 and 3 mug/ml of added cholesterol (Figure 5B). | |
| 0.95 | Dhcr24 becomes profoundly repressed (>95%), while Hmgcr mRNA remains expressed at approximately 30% of the levels observed in cholesterol-starved cells. | |
| 0.60 | Dhcr24, Scd2, Fasn and Hmgcr genes in cholesterol-depleted peritoneal macrophages under control, GW3965 or desmosterol treatment (6hr). | |
| 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. | |
| 19115107 | 0.98 | DHCR24-/- mouse brains compared to cholesterol in control brains might be an inhibiting effect of accumulating sterol intermediates of the Bloch-pathway on the HMG-coA-reductase, a rate-limiting enzyme in the cholesterol biosynthesis pathway. |
| 19183246 | 0.98 | 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. |
| 20804844 | 0.98 | 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA) and DHCR24 are strongly expressed in hair follicles. |
| 22855714 | 0.98 | Hmgcr, Fdft1, Dhcr24, Sqle and Idi1) and in the uptake of extracellular cholesterol (Ldlr) (Fig. 5B). |
| 25739789 | 0.98 | Hmgcr, Sqle, Dhcr24, Tm7sf2), together with Srebf2 (Fig. 3a). |
| 26067871 | 0.98 | Hmgcr, Hsd17b7, and Dhcr24) and transport (Abca1 and Abcg1) of cholesterol were up-regulated. |
| 26660104 | 0.98 | HMGCoAR, increase in DHCR24) and degradation (increase in CYP46A1) have altered expression in cultured H63D-HFE cells and H67D neuronal tissue, indicative of decreased cholesterol production and an increase in cholesterol efflux from the brain. |
| 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). |
| 30659202 | 0.98 | Dhcr24, Gpam, Hmgcr or Pck1), consistent with E47's known function as a lineage determining pioneer factor providing chromatin accessibility. |
| 31922003 | 0.98 | DHCR24, HMGCR, and LDLR, as well as fatty acid metabolism genes SREBP-1c, FASN, ACC-1, and SCD-1 after PMFE treatment (Fig. 1E). |
| 32111832 | 0.98 | Hmgcr, Sqs, Dhcr24, Pcsk9, and Ldlr (Fig. 4c). |
| 29033131 | 0.96 | Hmgcr or Dhcr24 had augmented capacity to stimulate IL-17A production from T cells, whereas this capacity was lost in the setting of ASC-deficiency (Fig. 3B). |
| 0.86 | HMG-CoA reductase (Hmgcr) and dehydrocholesterol 24-reductase (Dhcr24), enzymes in the cholesterol biosynthetic pathway, into BMDMs. | |
| 0.74 | Hmgcr and Dhcr24 mRNAs on caspase-1 was observed in the absence of an exogenous second signal. | |
| 29632203 | 0.96 | Dhcr24, Hmgcr, and Ldlr) while GW3965 and T0901317 activate Fasn and Srebf1 (Fig. 5B). |
| 25378657 | 0.89 | HMGCR, 3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS), and DHCR24, were not significantly different in the three genetically modified lines of mice from those of WT mice. |
| 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. |
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