Publication for Ldlr and Lipg
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Ldlr | low density lipoprotein receptor | 16835 | [link] | ||
| mmu | Lipg | lipase, endothelial | 16891 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 20034506 | 0.97 | lipase activity data indicate that plasma VLDL accumulation is likely a consequence of decreased VLDL clearance due to hepatic lipase and LDLR down-regulation more so than a consequence of increased lipid synthesis in part because several genes of cholesterol biosynthesis, including HMG-CoA reductase, also were down-regulated. |
| 26619823 | 0.97 | lipase activities of these genes might contribute to decreased hepatic lipid content in LD-fed Elovl6-/-Ldlr-/- mice. |
| 19632679 | 0.96 | lipase could function as ligand for VLDL uptake by the other hepatocyte receptor of the LDLR family, LRP. |
| 0.95 | LDL receptor, the VLDL acted upon in the plasma by lipase is readily cleared from the plasma accounting for the reduction in plasma triglyceride and VLDL despite increased hepatic production. | |
| 0.95 | LDLR-/- mice fed a Western-type diet, the plasma triglyceride and VLDL was notably increased, even in the face of an increase in plasma lipase activity. | |
| 28970555 | 0.90 | EL in atherosclerosis still remains inconclusive: in one study using apolipoprotein E (apoE)-deficient mice it has been shown that EL deficiency attenuates the progression of atherosclerosis, whereas in another study EL had no impact on atherosclerosis development in apoE- or LDL receptor-deficient mice. |
| 24747115 | 0.83 | Lipase, Macrophages and Atherosclerosis in LDLR-/- Mice |
| 23723371 | 0.59 | EL expression does not affect atherosclerosis in either ApoE-/- mice or LDLR-/- mice, even though plasma HDL-C levels are elevated. |
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