Publication for Ldlr and Acly

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Ldlr	low density lipoprotein receptor	16835			[link]
mmu	Acly	ATP citrate lyase	104112

Pubmed ID	Priority	Text
27892461	0.98	ACL leads to LDL receptor upregulation, decreased LDL-C and attenuation of atherosclerosis, independently of AMPK.
	0.98	ACL activity leads to a reduction in cytosolic acetyl-CoA, a required precursor for cholesterol and fatty acid synthesis, and subsequent compensatory LDL receptor upregulation.
	0.98	ACL by ETC-1002-CoA results in the suppression of cholesterol synthesis and compensatory LDLR upregulation and LDL particle clearance from the blood.
	0.97	LDL receptor activity (Fig. 5i), and in support of our clinical findings, the addition of ETC-1002 to atorvastatin increased LDL receptor activity above atorvastatin treatment alone, supporting that the co-suppression of ACL and HMG-CoA reductase activity is complementary (Fig. 5i).
	0.97	ACL activity to supply substrate for cholesterol biosynthesis and demonstrate an important regulatory link between ACL activity and LDL receptor regulation, thus demonstrating that ACL inhibition is a novel molecular target to reduce LDL-C.
	0.97	ACL by ETC-1002 leads to reduced cholesterol biosynthesis and the upregulation of LDL receptor expression in PHH, and Apoe-/- and DKO mice in vivo.
	0.96	ACL as a viable target for therapeutic intervention by reducing hepatic cholesterol synthesis and increasing LDL receptor activity.
	0.92	Acly siRNA resulted in an 80% reduction in ACL protein (Fig. 5j), which corresponded to more than a 50% increase in LDL receptor protein (Fig. 5j) and a 4-fold increase in LDL receptor activity (Fig. 5k).
	0.88	ACL activity by ETC-1002 was sufficient to trigger LDL receptor upregulation.
	0.68	ACL suppression increases LDLR activity
22197325	0.98	Ldlr-/-) mice showed increased expression of genes involved in FA synthesis, elongation, glycerolipid formation, and lipid storage, including Fasn, Acly, and Gpam (Figure 3B-C, Table S2).
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).
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).
30214638	0.97	Acly, Lss, and Sqle) and cholesterol transport (Stard4 and Ldlr).
29738536	0.95	Acly (ATP Citrate Lyase), Dhcr24 (24-Dehydrocholesterol Reductase), Hmgcs (HMG-CoA Synthase), 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	0.92	Acly, Fasn, Elovl5, Elovl6, Ucp2, Acss2, Acsl5, Ces3, Fabp4, Mvk, Mvd, Insig1, Ppap2a, Dgat2, Ppap2c, Pcsk9, Lpl, Gk2, Apoa4, Cd36 and Ldlr) involved in lipogenesis, lipid transport, lipid storage, bile acid biosynthesis, fatty acid synthesis, fatty acid oxidation, fatty acid catabolism, cholesterol biosynthesis, cholesterol transport, cholesterol homeostasis and triglyceride synthesis, indicating that the decreased expression of hepatic genes involved in lipid metabolism might be responsible, or contribute to the altered hepatic and serum lipid profiles (Fig. 8).
26311497	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.
29056891	0.86	ATP-citrate lyase (Acly), fatty acid synthase (Fasn), low-density lipoprotein receptor (Ldlr), peroxisomal acyl-coenzyme A oxidase 1 (Acox1), and forkhead box O1 (Foxo1).
19014463	0.79	ATP-citrate lyase, Fatty acid synthase, Stearoyl CoA desaturase 1, cholesterol synthesis and uptake genes, HMG CoA reductase, LDL receptor and Egr-1 transcription factor gene, that are also activated by IGF-1 in this study.