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Validated All-in-One™ qPCR Primer for NR1H3(NM_005693.3) Search again
Product ID:
HQP089999
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
LXR-a, LXRA, RLD-1
Gene Description:
nuclear receptor subfamily 1 group H member 3
Target Gene Accession:
NM_005693.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- data suggest a model in which LXR ligands trigger an autoregulatory loop leading to selective induction of hLXRalpha gene expression
- studies demonstrate that activated LXR induces the expression of the apoE/C-I/C-IV/C-II gene cluster in both human and murine macrophages
- Different regulation of the LXRalpha promoter activity by isoforms of CCAAT/enhancer-binding proteins
- interaction of peroxisome proliferator-activated receptor alpha with liver X receptor alpha antagonizes the stimulatory effect of their respective ligands on the murine cholesterol 7alpha-hydroxylase gene promoter
- LXRa is regulated by fatty acids in human cells
- SHP is able to interact with LXR and to modulate its transcriptional activity.
- PGC-1 alpha serves as a co-activator for the liver X receptor (LXR) alpha
- These data enable the identification of the amino acids that coordinate the interaction of both steroidal and non-steroidal ligands in the ligand-binding pocket of liver X receptor alpha.
- hLXRalpha and hLXRgeta transactivated a reporter gene bearing a truncated FPPS promoter containing a putative direct repeat 4 (DR4) LXR response element, and direct interaction was demonstrated
- LXRalpha and LXRbeta regulate transcription of the vascular endothelial growth factor gene in macrophages
- unliganded TRbeta1 suppresses promoter activity driven by LXRalpha and its ligand, whereas transactivation by T3-bound TRbeta1 is not affected by LXRalpha in the presence or absence of oxysterols
- LXRalpha plays an important role in the cAMP-mediated regulation of human renin gene transcription by binding to cAMP responsive element in the promoter.
- LXRs are expressed and functional in primary human coronary artery smooth muscle cells; their ligands inhibit cell proliferation and neointima formation
- activation of the liver X receptors (LXR) dramatically promoted lipid accumulation in vascular smooth muscle cells
- In the human body, the LXRalpha protein is highly expressed in macrophage lineage cells and foam cells in atherosclerotic lesions
- The beneficial effect of hepatic LXRalpha was abrogated by a synthetic LXR agonist, which activated SREBP-1c and its target genes.
- liver X receptor-alpha in mouse kidney and HK-2 proximal tubular cells is downregulated by LPS and cytokines
- expression of alternative LXRalpha transcripts in certain biological contexts may impact LXR signaling and lipid metabolism
- LXRalpha is a negative modulator of Abcd2, acting through a novel regulatory mechanism involving overlapping SREBP and LXRalpha binding sites
- competitive binding of coactivators and corepressors can explain the tissue-specific behavior of partial liver X receptor alpha and beta agonists
- LXR agonists may lead to increased utilisation of lipids and glucose in muscle cells without affecting the mechanism of action of insulin.
- Data demonstrate that LXR-alpha activation altered all of the cellular cholesterol fluxes.
- LXR-alpha gene plays a crucial role in the regulation of innate immunity at the genomic level.
- Results provide evidence that liver X receptors alpha and beta are phosphorylated proteins.
- Data show that liver X receptor alpha regulates the low-density lipoprotein receptor gene, which mediates the endocytic uptake of LDL cholesterol in the liver.
- in the investigated German sample, no evidence of association of ABCB11 and LXRA to gallstone susceptibility was detected. The gallstone trait is not allelic to progressive familial cholestasis at the ABCB11 locus.
- myeloperoxidase is regulated by LXR and PPARalpha ligands
- LXR-alpha and LXR-beta independently interfere with the hypothalamic-pituitary-adrenal axis regulation at the level of the pituitary and the adrenal gland
- One LXRA single nucleotide polymorphism, rs2279238, and one common haplotype, CAAGCC, as well as two LXRB single nucleotide polymorphisms, LB44732G>A and rs2695121, were associated with obesity phenotypes.
- novel mechanism of inflammatory gene regulation (C-reactive protein) by LXR ligands
- ROS and NF-kappaB, but not LXR, mediate the IL-1beta-induced downregulation of ABCA1 via a novel transcriptional mechanism, which might play an important role of proinflammation in the alteration of lipid metabolism.
- These studies define parallel but functionally distinct pathways that are utilized by PPARgamma and LXRs to differentially regulate complex programs of gene expression that control immunity and homeostasis.
- LXR is a potent modulator of dendritic cells maturation and function mediated in part by blocking the expression of fascin.
- LXRalpha is regulated not only by oxysterol derivatives but also by PKA-mediated phosphorylation, which suggests that nutritional regulation of SREBP-1c and lipogenesis could be regulated at least partially through modulation of LXR
- Results suggest that co-repression of LXR activity by RIP140 involves an atypical binding mode of RIP140 and a repression element in the RIP140 C-terminus.
- These data indicate for the first time that human macrophage aP2 promoter is a direct target for the regulation by LXR/RXR heterodimers.
- We show here that primary hASM cells express liver X receptor (LXR; alpha and beta subtypes), an oxysterol-activated nuclear receptor that controls expression of genes involved in lipid and cholesterol homeostasis, and inflammation.
- The LXR agonist T0901317, therefore, acts as an antiandrogen in human prostate cancer cells.
- Haplotype 2 associated with reduced mortality from infectious disease. Haplotype 2 also associated with higher levels of plasma apolipoprotein E, a target gene of the LXRalpha (p =.018), and higher levels of triglycerides (p =.041).
- This novel insight that thyroid hormone regulates LXR-alpha mRNA levels and promoter activity should shed light on a cross talk between LXR-alpha and TR-beta1 as a new therapeutic target against dyslipidemia and atherosclerosis.
- atorvastatin reduces LPL and EL expression by reducing the activation of LXRalpha and NF-kappaB, respectively
- It was proposed that LXR is a key regulator of cytokine release in LPS-challenged human monocytes, possibly by interfering with translational events.
- In summary, this study is the first to demonstrate anti-inflammatory actions of LXRs in the lung.
- LXRalpha and LXRbeta are expresed in the majority of the cell types in human skin.
- important roles of LXRalpha in differentiation and inflammatory signaling in sebaceous glands
- Upregulation of ABCG5/ABCG8 in gallstone patients, possibly mediated by increased liver X receptor (LXR) alpha, may contribute to the cholesterol supersaturation of bile, a prerequisite for gallstone formation.
- May modulate the bile acid biosynthetic pathway at a unique site downstream of cholesterol 7-alpha- ydroxylase (CYP7A1) and 3 alpha-hydroxysteroid dehydrogenase (AKR1C4) and may also modulate the metabolism of steroid hormones and certain xenobiotics.
- Laminar flow increases LXR function via a PPARgamma-CYP27 dependent mechanism, which reveals an atheroprotective role for laminar flow exerting on endothelium.
- review of role of activation of PPARalpha, -beta/delta, or -gamma or LXRs in skin physiology and cytology and disease
- results suggest that NR1H3 plays an important role in the HDL-cholesterol metabolism and in the genetic susceptibility to metabolic syndrome.
- reveal a previously unrecognized role for phosphorylation in restricting the repertoire of LXRalpha-responsive genes
- LXR (as a heterodimer with the retinoid X receptor) is able to bind the ENG promoter on an LXR response element and mediates the activation of ENG gene expression by LXRalpha in JAR cells.
- CRP modulates the expression of genes that contribute to both pro- and anti-inflammatory responses in human monocytes. Among these novel anti-inflammatory effects, we show clearly that CRP activates the LXRalpha pathway.
- These data identify Rev-erbalpha as a new LXR target gene, inhibiting LXR-induction of TLR-4 in a negative transcriptional feedback loop, but not cholesterol homeostasis gene expression.
- FXRalpha down-regulates CETP gene expression via binding to the DR4RE sequence within the CETP 5' promoter and this FXRalpha binding is essential for FXRalpha inhibition of LXRalpha-induced CETP expression.
- Data show that, at sufficiently high concentration, the NR corepressor (NCoR) influences the activity of the liver X receptor (LXR) even in the presence of a potent full agonist that destabilizes NCoR binding.
- 25-Hydroxycholesterol-3-sulfate regulates macrophage lipid metabolism via the LXR/SREBP-1 signaling pathway.