Publication for Ldlr and Elovl6

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
mmu Ldlr low density lipoprotein receptor 16835 [link]
mmu Elovl6 ELOVL family member 6, elongation of long chain fatty acids (yeast) 170439

Pubmed ID Priority Text
26619823 0.98 Elovl6 in Ldlr-/- mice was associated with an increased concentration of chenodeoxycholic acid (CDCA) in an LD-fed state (see Supplementary Fig. S2 online).
0.98 Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice (Fig. 6A).
0.98 Elovl6-/-Ldlr-/- mice compared to LD Elovl6+/+Ldlr-/- mice.
0.98 Elovl6+/+Ldlr-/- mice (Fig. 8A).
0.98 Elovl6-/-Ldlr-/- mice is the suppression of esterification of cholesterol secondary to decreased oleate (C18:1) levels in the liver.
0.98 Elovl6-/-Ldlr-/- mice resulted in supersaturation, precipitation and crystallization of cholesterol.
0.97 Elovl6-mediated changes in hepatic FA composition, especially oleic acid (C18:1n-9), control handling of hepatic cholesterol and BA, which protects against hepatotoxicity and steatohepatitis, but promotes gallstone formation in LD-fed Ldlr-/- mice.
0.97 Elovl6 abolished LD-induced gallbladder enlargement, indicating a decrease in the amount of bile in Elovl6-/-Ldlr-/- mice.
0.97 Elovl6+/+Ldlr-/- mice, but was significantly upregulated in the livers of LD-fed Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice.
0.97 Elovl6+/+Ldlr-/- mice.
0.97 Elovl6+/+Ldlr-/- mice, but significantly decreased in LD-fed Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice (Fig. 8B).
0.97 Elovl6+/+Ldlr-/- mice but suppressed in LD-fed Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice (Fig. 8C).
0.97 Elovl6 deficiency significantly attenuated LD-induced c-Jun N-terminal kinase (JNK) activation and alpha-smooth muscle actin (alpha-SMA) levels in Ldlr-/- mice (Fig. 8D,E).
0.97 Elovl6 gene product strongly inhibits LD-induced accumulation of hepatic and plasma cholesterol and plasma TBA in Ldlr-/- mice.
0.97 Elovl6 ameliorated LD-induced accumulation of lipids and BA in Ldlr-/- mice, indicating that Elovl6 and FA composition play a role in cholesterol and BA handling in hepatocytes.
0.97 Elovl6-/-Ldlr-/- mice.
0.97 Elovl6-/-Ldlr-/- mice are more susceptible to gallstone formation as a result of an alteration in hepatic cholesterol metabolism that promotes hepatic free cholesterol secretion into bile, coupled with alterations in hepatic BA metabolism.
0.96 Ldlr-/- mice on an LD, was reduced and HDL cholesterol was increased in LD-fed Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice (Fig. 2E).
0.96 Elovl6 modified the FA profiles of total lipid, cholesterol ester (CE), TG and PL fractions in the livers of Ldlr-/- mice fed an SD or an LD (Fig. 5).
0.96 Elovl6-/-Ldlr-/- mice compared with SD-fed Elovl6+/+Ldlr-/- mice (Fig. 5D).
0.96 Elovl6 deficiency significantly decreased the ratio of TDCA and TalphaMCA and significantly increased the ratio of glycocholic acid (GCA) in the livers of LD-fed Ldlr-/- mice.
0.96 Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice.
0.96 Elovl6-/-Ldlr-/- mice might compensate for the unbalanced FA composition.
0.96 Elovl6+/+Ldlr-/- mice.
0.96 Elovl6-/-Ldlr-/- mice.
0.96 Ldlr-/- mouse model, the reduction of oleate by Elovl6 deficiency is further reflected in CE formation.
0.96 Elovl6-/-Ldlr-/- mice.
0.96 Elovl6-/-Ldlr-/- mice in concert with decreased expression of Abcc1 and Abcc4.
0.95 Elovl6+/+Ldlr-/- mice (Fig. 1C).
0.95 Elovl6+/+Ldlr-/- mice were markedly elevated compared with levels in SD-fed Elovl6+/+Ldlr-/- mice as a consequence of dietary loading of cholesterol, fat and cholic acid (CA) in the LD.
0.95 Elovl6 deficiency was reflected in a significantly lower hepatic lobular inflammatory grade (evaluated by the number of inflammatory foci in hematoxylin & eosin [H&E]-stained liver sections) and plasma alanine aminotransferase (ALT) levels in LD-fed Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice (Fig. 4B,C).
0.95 Elovl6-/-Ldlr-/- mice compared with Elovl6+/+Ldlr-/- mice.
0.95 Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice; whereas, expression of diacylglycerol O-acyltransferase 1 (Dgat1) was similar in both genotypes.
0.95 Elovl6+/+Ldlr-/- mice, but was restored by the absence of Elovl6 (Fig. 6C).
0.95 Elovl6-/-Ldlr-/- mice compared with Elovl6+/+Ldlr-/- mice fed on both an SD and an LD.
0.95 Elovl6-/-Ldlr-/- mice.
0.95 Elovl6-/-Ldlr-/- mice have a greater ability to remove BAs from the hepatic-portal circulation than LD-fed Elovl6+/+Ldlr-/- mice.
0.94 Elovl6 suppresses hepatic lipid accumulation, plasma total cholesterol and total bile acid (BA) levels in LDL receptor-deficient (Ldlr-/-) mice challenged with a LD.
0.94 Elovl6+/+Ldlr-/- mice, the total lipid fractions of SD-fed Elovl6-/-Ldlr-/- mice had increased C16:0 and C18:2n-6 and decreased C20:3n-6, C22:0 and C24:0 (Fig. 5A).
0.94 Elovl6+/+Ldlr-/- mice, the total lipid fractions of LD-fed Elovl6-/-Ldlr-/- mice had increased C16:0 and a tendency toward decreased C18:1n-9.
0.94 Elovl6+/+Ldlr-/- mice, but was upregulated in LD-fed Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice.
0.94 Elovl6 deficiency suppresses lithogenic diet (LD)-induced hepatic lipid accumulation in Ldlr-/- mice.
0.93 Elovl6-/-Ldlr-/- mice that suppressed hepatic cholesterol and triglycerides accumulation and enhanced gallstone formation, rather than a functional change in the gallbladder or intestine.
0.92 Elovl6+/+Ldlr-/- mice exhibited significant reductions in epididymal white adipose tissue (WAT) weight compared with SD-fed Elovl6+/+Ldlr-/- mice (Fig. 1D).
0.92 Elovl6+/+Ldlr-/- mice and restored in Elovl6-/-Ldlr-/- mice.
0.92 Elovl6+/+Ldlr-/- mice, whereas the expression of these genes remained unchanged in LD-fed Elovl6-/-Ldlr-/- mice.
0.92 Elovl6-/-Ldlr-/- mice to gallstones.
0.91 Elovl6-/-Ldlr-/- mice displayed a complete lack of Slc10a1 and Slco1a1 suppression.
0.90 Elovl6+/+Ldlr-/- and Elovl6-/-Ldlr-/- mice compared with their SD-fed counterparts, but Elovl6-/-Ldlr-/- mice showed less LD-induced liver weight gain compared with Elovl6+/+Ldlr-/- mice (Fig. 1B).
0.90 Elovl6+/+Ldlr-/- mice after 4 weeks of the LD, the LD-fed Elovl6-/-Ldlr-/- mice had opaque gallbladders and increased numbers of aggregated cholesterol gallstones in greenish bile.
0.90 Elovl6+/+Ldlr-/- mice.
0.89 Elovl6+/+Ldlr-/- mice, the livers of the LD-fed Elovl6-/-Ldlr-/- mice had a decreased relative amount of C18:1n-9, whereas the relative amount of C16:0 was increased (Fig. 5B).
0.89 Elovl6-/-Ldlr-/- mice.
0.88 Elovl6-/-Ldlr-/- mice compared with LD-fed Elovl6+/+Ldlr-/- mice.
0.87 Elovl6 in Ldlr-/- mice had little effect on liver BA composition, except that the ratio of tauro-alpha-muricholate (TalphaMCA) was significantly decreased in the livers of Elovl6-/-Ldlr-/- mice compared with Elovl6+/+Ldlr-/- mice.
0.85 Elovl6+/+Ldlr-/- mice, LD-fed Elovl6-/-Ldlr-/- mice had significantly lower plasma TC, and plasma TBA levels were markedly suppressed (Fig. 2A, D).
0.85 Elovl6-/-Ldlr-/- mice compared with SD-fed Elovl6+/+Ldlr-/- mice (Fig. 5C).
0.81 Elovl6 deficiency suppresses hepatic lipid accumulation but promotes cholesterol crystallization and gallstone formation in Ldlr -/- mice
0.81 Elovl6+/+Ldlr-/- mice, but markedly ameliorated in LD-fed Elovl6-/-Ldlr-/- mice.
0.81 Elovl6 deletion attenuates the inflammatory response and hepatic injury in LD-fed Ldlr -/- mice
0.80 Elovl6 attenuates steatohepatitis but promotes gallstone formation in a lithogenic diet-fed Ldlr-/- mouse model
0.79 Elovl6-/-Ldlr-/- mice, the liver TC increase was reduced to half that observed in Elovl6+/+Ldlr-/- mice and there was no increase in TG levels (Fig. 3D, E).
0.79 Elovl6 deficiency alters bile acid composition in the livers and bile of Ldlr -/- mice
0.74 Elovl6 deficiency leads to decreased hepatic C18:1 in LD-fed Ldlr -/- mice
0.70 Elovl6 deficiency reduces plasma total cholesterol and bile acid levels in LD-fed Ldlr -/- mice
0.70 Elovl6-/-Ldlr-/- mice were strongly resistant to these changes caused by the LD.
0.66 Elovl6+/+Ldlr-/- and LD-fed Elovl6-/-Ldlr-/- mice.
0.63 Elovl6 in Ldlr-/- mice had little effect on BA composition in plasma despite strong suppression of the total BA level.
0.60 Elovl6+/+Ldlr-/- and Elovl6-/-Ldlr-/- mice (Fig. 2A-D).
0.60 Elovl6-/-Ldlr-/- mice (80%) than in Elovl6+/+Ldlr-/- mice (37.5%) after 4-week feeding of LD (Fig. 3B).
0.53 Elovl6 deficiency on body and tissue weight alterations in LD-fed Ldlr -/- mice
0.51 Elovl6-/-Ldlr-/- mice were further examined by measuring stresses and proinflammatory pathways.
31749969 0.97 ELOVL6 and ACCalpha were significantly lower in IL-1alpha KO compared with Loxp mice (figure 6A), with similar levels of DGAT, LXR, Srebpf-1c, ChREBP, HMGCR, Cyp7a and LDLR (Fig. 6A and online supplementary fig. S1).
0.78 ELOVL6), acetyl-CoA carboxylase alpha (ACCalpha), diacylglycerol acyltransferase (DGAT), the primary regulators of DNL including liver X receptors (LXR), sterol regulatory element-binding protein-1c (Srebpf-1c) and carbohydrate response element binding protein (ChREBP), and cholesterol metabolism related genes such as 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), cholesterol 7 alpha-hydroxylase (Cyp7a) and LDL receptor (LDLR).
24714086 0.97 ELOVL6 mRNA expression has been observed in NASH animal models, such as low-density lipoprotein receptor knockout animals fed a western type diet or a fructose diet.
26901190 0.95 low-density lipoprotein (LDL) receptor gene in knockout mice and concluded that the expression of miR-302 inhibited the expression of ELOVL6.
25799309 0.92 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).



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