Publication for Fdft1 and Ldlr
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Fdft1 | farnesyl diphosphate farnesyl transferase 1 | 14137 | [link] | ||
| mmu | Ldlr | low density lipoprotein receptor | 16835 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 22855714 | 0.98 | Fdft1, Dhcr24, Sqle and Idi1) and in the uptake of extracellular cholesterol (Ldlr) (Fig. 5B). |
| 23275357 | 0.98 | FDFT1 gene in the liver of both wild-type and LDLR knockout mice resulted in increased de novo cholesterol biosynthesis, oversecretion of cholesterol-rich LDL, higher cholesterol levels, and a 37% increase in liver weight compared with controls attributable to hepatocyte proliferation. |
| 23838163 | 0.98 | squalene synthase, and LDLR was higher with OS than PS (Figure 1C). |
| 25550450 | 0.98 | LDLR and squalene synthase (Figure 1B). |
| 26311497 | 0.98 | LDL receptor (LDLR) and squalene synthase (SS) (Fig. 1c). |
| 29500098 | 0.98 | squalene synthase, and the low-density lipoprotein (LDL) receptor. |
| 31327168 | 0.98 | Fdft1, Ldlr, and Sqle (Figure 2A). |
| 32111832 | 0.98 | Sqs, Dhcr24, Pcsk9, and Ldlr (Fig. 4c). |
| 22441164 | 0.97 | 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. |
| 24324835 | 0.97 | Ldlr) and fatty acid and cholesterol synthesis (Hmgcs1, Hmgcr, Fdps, Fdft1, Acly, Fasn), and down regulates genes involved in lipoprotein secretion (ApoA4, ApoA5, Mttp), fatty acid uptake and elongation (Elovl3, Pnpla2), intracellular transport of cholesterol (Npc1), mitochondrial transfer of acyl CoA (Cpt2, Crot, Crat, Slc25a20) and beta oxidation (Acox1, Acox2, Acadm, Acadvl, Hadhb, Ech1, Acaa1) (Table S3). |
| 27168937 | 0.97 | fdft1, fdps, hmgcs1, insig1, ldlr, lss, mvk, sc4mol, sc5dl, sqle) that Schmidt et al. (2009) identified as differently expressed in response to conditional knockout of por in mice, a cytochrome P450 that is essential for steroidogenesis (Fluck et al. 2004), were coordinately upregulated in our study at 22-24 DPA. |
| 28395113 | 0.97 | squalene synthase, and LDLR) and other lipid transport genes (adenosine triphosphate-binding cassette transporter A 1 and ACAT2) was reduced in CRTC2-/- mice (Fig. 5D). |
| 28459857 | 0.97 | Fdft1, Sqle and Ldlr, while the expression of ApoE was reduced by more than six-fold (data not shown). |
| 31767163 | 0.95 | squalene synthase enzymes, as well as of LDLR and LRP1 (HMGCR: t(4) = 9.38, p = 0.007; FDFT1: t(4) = 17.43, p < 0.0001; LDLR: t(4) = 11.80, p = 0.0003; LRP1; t(4) = 0.60, p = 0.58). |
| 0.94 | LDLr also resulted in downregulation of HMGCR and FDFT1, albeit to a smaller extent. | |
| 29738536 | 0.95 | Ldlr (Low Density Lipoprotein Receptor), Fdps (Farnesyl Diphosphate Synthase), and Sqs (Squalene Synthase) and found that all were dose dependently upregulated by pravastatin (Fig 4C) as well as simvastatin (S4A Fig). |
| 22985096 | 0.93 | Fdft1, CYP51, Sc4mol, and Ldlr; ) for putative binding sites for the 13 downregulated miRNAs. |
| 25799309 | 0.87 | 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. |
| 25849138 | 0.50 | squalene synthase (Fdft1), Cyp51 and the LDL receptor (Ldlr) were also normalized in LIRKO mice by treatment with FMO3 ASO (Fig. 2j). |
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