Publication for Ldlr and Msmo1
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Ldlr | low density lipoprotein receptor | 16835 | [link] | ||
| mmu | Msmo1 | methylsterol monoxygenase 1 | 66234 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 26344763 | 0.98 | SC4MOL and NSDHL in A431 cervical carcinoma cells (Fig. 4B), while LDLR expression was decreased (Fig. 4C). |
| 0.98 | SC4MOL or NSDHL activates canonical LXR targets such as ABCA1, ABCG1, and represses LDLR, which regulate cellular release and uptake of cholesterol, respectively. | |
| 25147951 | 0.98 | Sc4mol, Fads2, Scd2, Stard4, 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. |
| 26938916 | 0.97 | LDLR, NSDHL, SC4MOL, SREBF2; S4F Table). |
| 0.96 | LDLR, NSDHL, SREBF2, SC4MOL) mostly differ with those in Bahd1-KO murine placentas (e.g. Apoc3, Atp8b1, Cyp11A1, Insig2, Osbpl5, Pbx1, VldlR). | |
| 0.83 | LDLR and SC4MOL correlated with obesity-related type 2 diabetes and cardiovascular diseases. | |
| 27168937 | 0.97 | 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. |
| 0.90 | ldlr, lss, mvk, pmvk, insig1, sc4mol, sc5dl, sqle) (Fig. 12I-L). | |
| 26226008 | 0.97 | SC4MOL), LDLR, and SRB1, and decreases cholesterol efflux and catabolism by suppressing ABCA1, ABCG1, ABCG5/G8, and CYP7A1. |
| 22985096 | 0.93 | Sc4mol, and Ldlr; ) for putative binding sites for the 13 downregulated miRNAs. |
| 25799309 | 0.87 | 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. |
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