Goat Anti-LXR beta / NR1H2 Antibody
Peptide-affinity purified goat antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC, E |
---|---|
Primary Accession | P55055 |
Other Accession | NP_009052, 7376 |
Reactivity | Human |
Predicted | Mouse, Rat, Dog |
Host | Goat |
Clonality | Polyclonal |
Concentration | 100ug/200ul |
Isotype | IgG |
Calculated MW | 50974 Da |
Gene ID | 7376 |
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Other Names | Oxysterols receptor LXR-beta, Liver X receptor beta, Nuclear receptor NER, Nuclear receptor subfamily 1 group H member 2, Ubiquitously-expressed nuclear receptor, NR1H2, LXRB, NER, UNR |
Format | 0.5 mg IgG/ml in Tris saline (20mM Tris pH7.3, 150mM NaCl), 0.02% sodium azide, with 0.5% bovine serum albumin |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | Goat Anti-LXR beta / NR1H2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | NR1H2 |
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Synonyms | LXRB, NER, UNR |
Function | Nuclear receptor that exhibits a ligand-dependent transcriptional activation activity (PubMed:25661920). Binds preferentially to double-stranded oligonucleotide direct repeats having the consensus half-site sequence 5'-AGGTCA-3' and 4-nt spacing (DR-4). Regulates cholesterol uptake through MYLIP-dependent ubiquitination of LDLR, VLDLR and LRP8; DLDLR and LRP8. Interplays functionally with RORA for the regulation of genes involved in liver metabolism (By similarity). Induces LPCAT3-dependent phospholipid remodeling in endoplasmic reticulum (ER) membranes of hepatocytes, driving SREBF1 processing and lipogenesis (By similarity). Via LPCAT3, triggers the incorporation of arachidonate into phosphatidylcholines of ER membranes, increasing membrane dynamics and enabling triacylglycerols transfer to nascent very low-density lipoprotein (VLDL) particles (By similarity). Via LPCAT3 also counteracts lipid-induced ER stress response and inflammation, likely by modulating SRC kinase membrane compartmentalization and limiting the synthesis of lipid inflammatory mediators (By similarity). Plays an anti-inflammatory role during the hepatic acute phase response by acting as a corepressor: inhibits the hepatic acute phase response by preventing dissociation of the N-Cor corepressor complex (PubMed:20159957). |
Cellular Location | Nucleus {ECO:0000255|PROSITE-ProRule:PRU00407}. |
Tissue Location | Ubiquitous. |
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Provided below are standard protocols that you may find useful for product applications.
Background
The liver X receptors, LXRA (NR1H3; MIM 602423) and LXRB, form a subfamily of the nuclear receptor superfamily and are key regulators of macrophage function, controlling transcriptional programs involved in lipid homeostasis and inflammation. The inducible LXRA is highly expressed in liver, adrenal gland, intestine, adipose tissue, macrophages, lung, and kidney, whereas LXRB is ubiquitously expressed. Ligand-activated LXRs form obligate heterodimers with retinoid X receptors (RXRs; see MIM 180245) and regulate expression of target genes containing LXR response elements (summary by Korf et al., 2009 [PubMed 19436111]).
References
Variation at the NFATC2 Locus Increases the Risk of Thiazolinedinedione-Induced Edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) Study. Bailey SD, et al. Diabetes Care, 2010 Jul 13. PMID 20628086. LXR activation inhibits chemokine-induced CD4-positive lymphocyte migration. Walcher D, et al. Basic Res Cardiol, 2010 Jul. PMID 20364260. Regulation of thyroid hormone activation via the liver X-receptor/retinoid X-receptor pathway. Christoffolete MA, et al. J Endocrinol, 2010 May. PMID 20176747. GPS2-dependent corepressor/SUMO pathways govern anti-inflammatory actions of LRH-1 and LXRbeta in the hepatic acute phase response. Venteclef N, et al. Genes Dev, 2010 Feb 15. PMID 20159957. Integrative predictive model of coronary artery calcification in atherosclerosis. McGeachie M, et al. Circulation, 2009 Dec 15. PMID 19948975.
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