Publication for Ldlr and Acat2

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Ldlr	low density lipoprotein receptor	16835			[link]
mmu	Acat2	acetyl-Coenzyme A acetyltransferase 2	110460

Pubmed ID	Priority	Text
21071704	0.98	Acat2, Lcat), and cholesterol uptake (Ldlr, SR-BI) were all significantly reduced in Hnf4alpha-deficient mice (Figure 2A).
	0.97	Ldlr, SR-BI (cholesterol uptake), Acat2, Lcat (cholesterol esterification), Abca1, Abcg5, Abcg8 (transporters), Apoa1, Apoa2, and Apoc2 (apolipoproteins) (Table 1).
30580099	0.98	Ldlr, Pcsk9, Hmgcr, Hmgcs1, Pmvk and Acat2 (Fig. 3F).
24695360	0.97	ACAT2 was reduced, independently of the levels of Abca1 mRNA expression; an effect also seen in apoB100only-LDLr-/- mice.
	0.96	LDLr knockout mice an increase in HDL cholesterol was observed when ACAT2 was knocked out.
	0.96	ACAT2 KO mice was not different from that of their respective littermates, and ASO6 treatment led to a reduction of biliary cholesterol secretion in apoB100only-LDLr-/- mice.
26619823	0.97	Acat2 in the livers of Elovl6-/-Ldlr-/- mice might compensate for the unbalanced FA composition.
	0.94	acetyl-coenzyme A acetyltransferase 2 (Acat2) was increased in LD-fed Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice.
28395113	0.97	LDLR) and other lipid transport genes (adenosine triphosphate-binding cassette transporter A 1 and ACAT2) was reduced in CRTC2-/- mice (Fig. 5D).
	0.95	acetyl-coenzyme A acetyltransferase 2 (ACAT2, a cholesterol-esterifying enzyme26) were reduced in the livers of Ad-CRTC2 mice, while the LDLR levels were unchanged (Fig. 5A).
21812109	0.95	Ldlr, Lip1) and cholesterol efflux via VLDL (Acat2) were down-regulated, while apolipoprotein B mRNA was up-regulated.
19166320	0.94	ACAT2, SREBP, HMGR, and LDLR.
24505463	0.93	Acat2 with antisense oligonucleotides prevented dietary cholesterol-associated hepatic steatosis both in an inbred mouse model of non-alcoholic fatty liver disease (SJL/J) and in a humanized hyperlipidemic mouse model (LDLr-/-, apoB100/100), and ACAT2-specific inhibitors might hold unexpected therapeutic potential to treat both athero-sclerosisand non-alcoholic fatty liver disease.
23744992	0.90	ACAT-2, Ldlr CYP7A1 and SR-BI was assessed.
28380440	0.72	Ldlr, Srb1), cholesterol and bile acid (BA) excretion (Abcg1, Abcg5, Abcg8, Bsep), cholesterol and BA synthesis (Srebp2, HmgCoAr, Cyp7a1, Cyp27a1, Cyp8b1), and cholesterol esterification (Acat2).