Publication for Ldlr and Fdps

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Ldlr	low density lipoprotein receptor	16835			[link]
mmu	Fdps	farnesyl diphosphate synthetase	110196

Pubmed ID	Priority	Text
25147951	0.98	Ldlr, Insig-1, and Fdps, which are direct targets of SREBPs and involved in the cholesterol/lipid biosynthetic pathways, are down-regulated in S1Pcko cartilage (Table 2) mirroring that seen in the microarray.
	0.97	Ldlr, Fads2, and Fdps genes at the RNA level in the humerus of S1Pcko mice (Fig. 8).
	0.93	Ldlr, Fads2, and Fdps genes at the RNA level, shown by in situ hybridization in S1Pcko humerus and by immunohistochemistry (IHC) for Scd1 protein in S1Pcko femur.
30524198	0.98	farnesyl diphosphate synthetase (Fdps) (Figure 3(b), left panel), a key enzyme involved in isoprenoid biosynthesis and catalyzes the formation of several metabolic precursors, are significantly downregulated in LDLR-/-; macLRP1-/- peritoneal macrophages isolated from mice fed a chow diet.
	0.97	LDLR-/- and LDLR-/-; macLRP1-/- mice fed a standard chow or Western diet for two weeks revealed three genes that were differentially regulated: Fdps, Pcsk9, and Soat1 (Figure 4(b)).
	0.93	Fdps significantly dropped in LDLR-/- peritoneal macrophages compared to those on a chow diet, while levels remained unchanged in LDLR-/-; macLRP1-/- peritoneal macrophages regardless of diet.
29073233	0.98	Fdps and Ldlr, the cholesterol input genes and targets of transcriptional regulation by SREBF.
	0.93	Fdps, Ldlr, Cyp46a1, Akr1d1, and Cela3b) and 11 genes in the brain of male Cyp46a1-/- mice (Apoa2, Apoc3, Nr0b2, Npc1/1, Srebf2, Snx17, Cyp46a1, Nsdhl, Lipe, Il4, and Apoa4) showed more than a 2-fold change (an arbitrary cut off limit) in the expression level as compared to the expression of the genes in the brain of wild type animals (Fig 3).
23585733	0.98	Fdps, Idi1, and Ldlr) were all markedly down-regulated by 70%-90% (Figure 2E).
26964834	0.98	low density lipoprotein receptor (LDLR), 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), hydroxy-3-methylglutaryl-coenzyme A synthase 1 (HMGCS1), and farnesyl diphosphate synthase (FDPS).
29500098	0.98	farnesyl diphosphate synthase, squalene synthase, and the low-density lipoprotein (LDL) receptor.
30580099	0.98	Ldlr, Pcsk9, Srebp1c, farnesyl diphosphate synthetase (Fdps), ATP citrate lyase (Acly), steroid 17-alpha-monooxygenase (gene symbol Cyp17a1) were significantly repressed in the absence of hepatic ACSL1 (Fig. 5D), which corroborated our qRT-PCR results (Fig. 3F).
26311497	0.97	LDLR, FDPS, SS, ACC, FAS, SCD-1 and GPAT, but also ameliorated gene expression in SREBP pathway, including SREBP-1a, SREBP-1c, SREBP-2 and Insig-1,without change in Scap expression (Fig. 6b).
	0.90	LDLR, FDPS (farnesyl diphosphate synthase), SS, FAS (FA synthase), SCD-1 (stearoyl CoA desaturase-1), ACC (acetyl CoA carboxylase), ACLY (ATP citrate lyase), GPAT (glycerol-3-phosphate acyltransferase), SREBP-1c, SREBP-2, and Insig-1 were all lower in PAQR3-shRNA group than in the control mice.
27168937	0.97	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.
	0.89	fdps, hmgcs1, ldlr, lss, mvk, pmvk, insig1, sc4mol, sc5dl, sqle) (Fig. 12I-L).
22441164	0.97	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.
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).
29738536	0.94	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).
25799309	0.88	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.
25849138	0.73	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).