Publication for Ldlr and Srebf1
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Ldlr | low density lipoprotein receptor | 16835 | [link] | ||
| mmu | Srebf1 | sterol regulatory element binding transcription factor 1 | 20787 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 21459323 | 0.98 | SREBP-1c phosphorylation in vivo is evidence by the fact that SREBP-1c phosphorylation was diminished by AMPK impairment in insulin resistant LDLR-/- mice and stimulated by AMPK activation in S17384-treated mice. |
| 0.97 | LDL receptor deficient mice in part through phosphorylation of SREBP-1c Ser372 and suppression of SREBP-1c and -2-dependent lipogenesis. | |
| 0.97 | LDLR-/- mice treated with S17834, stimulates SREBP-1c phosphorylation, decreases cleavage of SREBP-1c and -2, and reduces expression of key target lipogenic enzymes, which in turn ameliorates insulin resistance, hepatic steatosis, hyperlipidemia, and atherosclerosis. | |
| 0.97 | LDLR-Luc reporter genes, comparable to its effects on SREBP-1c promoter (Fig. S5D-F). | |
| 0.94 | SREBP-1c precursor in the liver of insulin resistant LDLR-/- mice. | |
| 0.92 | SREBP-1 and SREBP-2, inhibits expression of their target lipogenic enzymes, and reduces lipid accumulation in the liver of the insulin resistant LDLR-/- mice | |
| 22666465 | 0.98 | SREBP-1 to the LDLR promoter is reduced in DJ-1-knockdown cells, DJ-1 may affect binding activity of SREBP-1 by unknown mechanism. |
| 0.98 | SREBP-1 to the LDLR promoter was reduced in DJ-1-knockdown cells (Figure 5A-b), DJ-1 may affect binding activity of SREBP-1 by unknown mechanism. | |
| 0.97 | SREBP-1, significantly reduced expression levels of LDLR mRNA. | |
| 0.97 | LDLR promoter to activate its promoter activity and that SREBP-1 also binds to the SRE without complex formation with DJ-1. | |
| 0.97 | LDLR promoter to activate its promoter activity and that SREBP-1 also binds to the SRE without complex formation with DJ-1. | |
| 0.91 | SREBP-1 do not significantly reduce the expression level of LDLR mRNA in DJ-1-knockdown D2 cells (Figure 6C). | |
| 31327168 | 0.98 | SREBP1 drives the expression of a gene that mediates the degradation of LDLR by elaidate. |
| 0.97 | LDLR protein levels, which is independent of SREBP2 and dependent on SREBP1 and SCAP. | |
| 0.97 | LDLR protein levels, via a mechanism independent of SREBP2 and dependent on SREBP1. | |
| 0.97 | SREBP1 rather than SREBP2 appears to be the primary regulator of LDLR in Hepa1-6 cells. | |
| 0.92 | LDLR protein in Hepa1-6 cells treated with Srebp2 siRNA but not Srebp1 or Scap siRNA (Figure 3E). | |
| 19556020 | 0.98 | SREBP-1c preferentially controls the expression of genes involved in triglyceride synthesis and accumulation, such as fatty acid synthase (FAS) and acetyl coenzyme-A carboxylase (ACC), whereas SREBP-2 activity has been more closely linked to regulation of genes involved in cholesterol synthesis and uptake, such as low-density lipoprotein receptor (LDLR) and 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR). |
| 0.98 | LDLR was not increased, showing that SREBP-1 is indeed activated by SSW (Fig. 4C). | |
| 0.95 | LDLR and HMGCR were not, suggesting the activation of SREBP-1 but not SREBP-2 (Fig. 4A). | |
| 0.78 | SREBP-1 function but not that of SREBP-2, we performed RT-PCR on cells exposed to SSW and examined the expression of genes that are stimulated by the binding of the active forms of these SREBPs to their elements in the DNA, such as FAS and ACC for SREBP-1 and LDLR and HMGCR for SREBP-2. | |
| 18782462 | 0.98 | LDL receptor superfamily, along with similar programmed suppression of the mRNA expression of hepatic SREBP-1c. |
| 0.98 | LDLr gene expression and that SREBP1c may be a target for programming by maternal protein restriction. | |
| 0.87 | LDLr, LRP-1 and SREBP-1c mRNA expression in the liver were not directly associated with lesion area, LRP-1 expression was significantly related to plasma cholesterol concentrations (P=0.027). | |
| 27050512 | 0.98 | SREBP1 failed to downregulate Ldlr transcripts in mice, suggesting a potential post-translational regulation of LDLR independent of SREBP signaling. |
| 0.96 | LDLR protein expression (-64.7%), the precursor and mature SREBP1 were reduced by 49.1% and 53.8%, respectively, whereas the SREBP2 precursor was unaffected (Figure 3A). | |
| 0.79 | LDLR expression might also be under the control of SREBP1. | |
| 19592617 | 0.98 | Ldlr-/- controls, implying that the loss of SREBP1c-stimulated triglyceride synthesis was the primary determinant for reduced apoB secretion. |
| 0.96 | Ldlr-/- mice, the PPARalpha agonist fenofibrate increased hepatic expression of Aco and Lpl, while Srebp1c, Fas, and Dgat2 were reduced. | |
| 30863273 | 0.98 | LDLR for cellular uptake of LDL cholesterol and clearance of plasma cholesterol, whereas SREBP-1 seems to be involved in energy metabolism including fatty acid metabolism. |
| 0.95 | low-density lipoprotein receptor, adenosine triphosphate (ATP)-binding cassette A1, and ATP-binding cassette G1, while decreasing the protein expression of Niemann-Pick C1-like protein 1, SREBP-1, fatty acid synthase, and acetyl-coenzyme A carboxylase, which were involved in intestinal cholesterol metabolism. | |
| 30941042 | 0.98 | SREBP-1c), and subsequently increasing LDLR protein expression. |
| 0.98 | LDLR through SREBP-1c activation, and our study showed that Akt indeed influenced SREBP-1c expression (see Supplementary Figure S1). | |
| 18852694 | 0.98 | SREBP1 is responsible for fatty acid synthesis and metabolism, whereas SREBP2 controls expression of LDLR and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme for cholesterol synthesis (Brown and Goldstein, 1997; Shimano, 2001). |
| 19509018 | 0.98 | Ldlr-/- mice was associated with significant reduction in plasma adipose-derived FFA (Fig. 3A), glucose, and insulin (Fig. 4A and B), as well as with diminished expression of lipogenic master gene, sterol regulatory element-binding transcription factor 1 (Srebf1), and its key downstream target, fatty acid synthase mRNA and protein (Fig. 5B-D). |
| 23243415 | 0.98 | LDLR -/- mice displayed decreased mRNA levels in the liver of several genes involved in lipid metabolism (Srebp1a, Srebp1c, AbcA1, Lxralpha, and Cyp7b1). |
| 23528177 | 0.98 | SREBP-1a at Ser117 (Ser117corresponds to Ser92 in SREBP-1c); this event impairs insulin-stimulated regulation of the LDL receptor (LDLR) promoter by SREBP-1a. |
| 26046396 | 0.98 | SREBP1c (required for de novo lipogenesis and adipogenesis) and SREBP-2 (which activates cholesterol and LDLR biosynthesis) boost adipogenesis and VLDL assembly, resulting in hyperlipidemia and non-alcoholic fatty liver diseases. |
| 26555173 | 0.98 | SREBP-1 and SREBP-2 in a dose- and time-dependent manner and increased the protein levels of fatty acid synthase (FASN) and low-density lipoprotein receptor (LDLR), the genes encoding both of which are downstream targets for SREBP-1 (Figures 1B, 1C, S1A and S1B). |
| 29183708 | 0.98 | LDLR (IDOL), SREBP-1c, fatty acid synthase (FASN), phospholipid transfer protein (PLTP) and ADP-ribosylation factor (ARF)-like 7 (ARL7). |
| 29899496 | 0.98 | Ldlr-/-Sort1-/- mouse jejunum had reduced LXR-related (Nr1h3, Nr1h2, Rxra, Apoe, Abca1, Abcg1, Srebf1, Ppara, Sp1, Hnf4a) and sterol-related (Hmgcr, Hmgcs1, Cyp27a1, Vldlr) mRNA levels (Fig. 5a and Supplementary Fig. S3c). |
| 30891077 | 0.98 | LDLR, SREBP1/2, CYP7A1, and ABCG5/8 (Figure 7). |
| 27834848 | 0.97 | SREBP1, SREBP2, and LDLR. |
| 0.95 | Sterol regulatory element binding proteins 1 (SREBP1), fatty acid synthase (FAS), peroxisome proliferator activated receptor-gamma (PPARgamma), SREBP2, low-density lipoprotein receptor (LDLR), and hydroxymethylglutaryl-coenzyme A reductase (HMGR) genes compared with OLZ alone. | |
| 0.95 | SREBP1, fatty acid synthetase (FAS) and PPARgamma) and cholesterogenesis (SREBP2, low-density lipoprotein receptor (LDLR) and hydroxymethylglutaryl coenzyme A reductase (HMGR)). | |
| 0.95 | SREBP1, SREBP2, and LDLR. | |
| 0.89 | SREBP1, SREBP2, and LDLR by 57.71% +- 9.42%, 73.05% +- 11.82%, and 59.46% +- 9.91%, respectively. | |
| 22384276 | 0.97 | SREBP-1a does not interfere with mRNA expression, maturation or protein/DNA interaction of SREBP-1a, but is related to ERK-MAPK pathway inducible increase of e.g. gene expression of SREBP-1a target genes like the LDLR and central genes of lipid metabolism in cell culture models. |
| 0.96 | LDLR or ABCA1 were increased 2.5-fold in alb-SREBP-1 aDeltaP mice and increased more than five- fold in alb-SREBP-1a mice. | |
| 26344763 | 0.97 | LDLR is, in part, stimulated by activated SREBP1. |
| 0.77 | SREBP1 and SREBP2, and depleted LDLR in A431 cells in vitro (Fig. 5G). | |
| 22363740 | 0.97 | LDLR or HMG-CoAR was up-regulated in livers of the alb-SREBP-1c animals and in cell models but unaltered in the livers of PEPCK-SREBP-1c mice. |
| 25155036 | 0.97 | LDLR, SCD-1, and DGAT-2 are all targets of SREBP-1c. |
| 28474500 | 0.97 | Srebp-1c, a transcription factor that regulates genes involved in lipogenesis, was significantly decreased in both, LDLR-/- and LDLR+/+, Vitamin D3 supplemented high fat high sugar diet groups. |
| 29587401 | 0.97 | SREBP-1 integrates the hormone signal also to transcriptional activation of DNL and also lipid transport via LDL receptor or VLDL assembling. |
| 22952870 | 0.96 | low density lipoprotein receptor (LDLR), sterol regulatory element-binding protein-1 (SREBP-1), sterol regulatory element-binding protein-2 (SREBP-2), SREBP-cleavage activating protein (SCAP), insulin-induced gene-1 (INSIG-1), site-1 protease (S1P), and site-1 protease (S2P). |
| 0.95 | LDLR, SREBP1C and SCAP mRNAs oscillate in the mouse liver | |
| 0.90 | LDLR, SREBP1, and SREBP1c expressions oscillated in the mouse liver under free-running condition that is in good agreement with previous reports. | |
| 22225954 | 0.96 | SREBP-1 in nuclear protein levels but not SREBP-2 both in C57BL/6 mice and LDLR-/- mice fed with HCD or HFD. |
| 23554170 | 0.96 | LDLR and HMGCS (see Supporting information Fig 4A and B), we hypothesized that increased expression of APP in neurons would inhibit proteolytic release of mSREBP1 and/or its nuclear translocation. |
| 23734208 | 0.96 | SREBP-1 was discovered as a transcription factor regulating low density lipoprotein receptor gene expression and coincidentally as adipocyte determination- and differentiation-dependent factor 1. |
| 24603306 | 0.96 | Ldlr, Pcsk9, Pparalpha, Ppargamma, Srebp1, and Srebp2 (Figure 3A). |
| 27499577 | 0.95 | SREBP-1, SCD-1, FAS, LDLR, and CYP7alpha1 in the liver. |
| 0.95 | SREBP-1, SCD-1, FAS, LDLR and CYP7alpha1 were enhanced by HFD. | |
| 0.94 | SREBP-1, SCD-1, FAS, HMGCR, LDLR, CYP7alpha1 and PPAR-alpha proteins in the liver; and the SREBP-1, SCD-1, FAS, PPAR-alpha and adiponectin proteins in adipose tissue were reversed by PGBR. | |
| 0.94 | SREBP-1 (56%), SCD-1 (130%), FAS (320%), LDLR (31%) and CYP7alpha1 (74%) proteins, compared with the SRD group. | |
| 0.91 | SREBP-1 (48%), SCD-1 (34%), FAS (57%), HMGCR (78%), and increase in LDLR (50%), CYP7alpha1 (66%) and PPARalpha (75%) protein levels compared with the HFD group (Fig. 1). | |
| 0.91 | SREBP-1, SCD-1, FAS, HMGCR, increasing LDLR, CYP7alpha1 and recovering adiponectin through regulating PPARs. | |
| 0.88 | SREBP-1, SCD-1, FAS, HMGCR, LDLR, CYP7alpha1, PPARalpha, and adiponectin in liver and adipose tissue were recovered by PGBR. | |
| 0.86 | SREBP-1, SCD-1, FAS, HMGCR, LDLR, CYP7alpha1 and PPARalpha protein expressions in liver of high-fat diet (HFD) fed mice. | |
| 19260826 | 0.95 | SREBP-1 and SREBP-2 processing (Figure 4A) and decreased Hmgcr, Ldlr and Insig1 mRNA levels (Figure 4B), although less potently than 25HC. |
| 0.93 | SREBP-1 and SREBP-2 processing as well as Hmgcr, Ldlr and Insig1 expression (Supplementary Figure S2). | |
| 31382500 | 0.95 | Ldlr-/- mice lacking Srebp1c. |
| 0.79 | Ldlr-/-/Srebp1c-/- mice as compared to Ldlr-/- mice. | |
| 26437365 | 0.95 | SREBP1 association was observed in an upstream region of the miR-148a promoter that lacked SREBP1 binding sites (uNEG), Moreover, we also found an enrichment of miR-148a and LDLR mRNA in the RISC complex of mice that were fasted and subsequently refed (Fig. 4j). |
| 28720427 | 0.95 | Ldlr-null mice while lowering plasma triglycerides, potentially also through inhibition of SREBP-1c activation. |
| 23580231 | 0.93 | SREBP1/2 targets, including the Low Density Lipoprotein Receptor (LDLR), HMG-CoA reductase, and PCSK9, remained unchanged by mRNA-seq and qPCR, though SCD1 was decreased by ~50% in Sec24agt/gt mice (Figure 5D), as observed by mRNA-seq (FDR < 3 x 10-13). |
| 26495026 | 0.92 | SREBP1aTg LDLR-/- mice exhibit marked increases in plasma Blp-c and triglycerides, whereas LDLR-/- S1Pf/fCre mice have decreased plasma Blp-c and triglycerides (Fig. 7). |
| 0.90 | LDLR whose function is enhanced by up-regulation of SREBP1a. | |
| 27417587 | 0.91 | sterol regulatory element binding protein-1 (SREBP-1) (Srebf1) and its target genes involved in lipogenesis were not induced in Ldlr-/- Creb3l3-/- mice, excluding the possibility of increased lipogenesis in these mice (Figure IIC in the online-only Data Supplement). |
| 18771980 | 0.89 | SREBP-1a, SREBP-2, HMGCR and LDLR, and to study the correlations between the expression of these mediators. |
| 21810592 | 0.85 | SREBP1c, an important regulator of FASN-directed lipogenesis, on the other hand, tended to be higher in the diabetic E4LDLR-/- livers but did not reach significance. |
| 0.62 | SREBP1c, SREBP2, FOXO1, ChREBP, PPARalpha, CPT1, and FASN in the livers of diabetic E3LDLR-/- and diabetic E4LDLR-/- mice. |
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