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NR1H3 Antibody (Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IF, FC, E |
|---|---|
| Primary Accession | Q13133 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 50396 Da |
| Antigen Region | 226-253 aa |
| Gene ID | 10062 |
|---|---|
| Other Names | Oxysterols receptor LXR-alpha, Liver X receptor alpha, Nuclear receptor subfamily 1 group H member 3, NR1H3, LXRA |
| Target/Specificity | This NR1H3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 226-253 amino acids from the Central region of human NR1H3. |
| Dilution | IF~~1:10~50 WB~~1:1000 FC~~1:10~50 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | NR1H3 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | NR1H3 |
|---|---|
| Synonyms | LXRA |
| Function | Nuclear receptor that exhibits a ligand-dependent transcriptional activation activity (PubMed:19481530, PubMed:25661920). Interaction with retinoic acid receptor (RXR) shifts RXR from its role as a silent DNA-binding partner to an active ligand-binding subunit in mediating retinoid responses through target genes defined by LXRES (By similarity). LXRES are DR4-type response elements characterized by direct repeats of two similar hexanuclotide half-sites spaced by four nucleotides (By similarity). Plays an important role in the regulation of cholesterol homeostasis, regulating cholesterol uptake through MYLIP-dependent ubiquitination of LDLR, VLDLR and LRP8 (PubMed:19481530). 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. 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). |
| Cellular Location | Nucleus {ECO:0000255|PROSITE-ProRule:PRU00407, ECO:0000269|PubMed:25661920}. Cytoplasm {ECO:0000250|UniProtKB:Q9Z0Y9} |
| Tissue Location | Visceral organs specific expression. Strong expression was found in liver, kidney and intestine followed by spleen and to a lesser extent the adrenals |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
NR1H3 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.
References
Davila, S., et al. Genes Immun. 11(3):232-238(2010)
Nedumaran, B., et al. J. Biol. Chem. 285(12):9221-9232(2010)
Zhao, C., et al. J. Endocrinol. 204(3):233-240(2010)
Anthonisen, E.H., et al. J. Biol. Chem. 285(3):1607-1615(2010)
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