Rabbit Recombinant Monoclonal NR1D1 antibody - conjugated to Alexa Fluor® 594.
IgG
Rabbit
Alexa Fluor® 594
Ex: 590nm, Em: 617nm
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 68% PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Liquid
Monoclonal
Application | Reactivity | Dilution info | Notes |
---|---|---|---|
Application Target Binding Affinity | Reactivity Expected | Dilution info - | Notes - |
Application Antibody Labelling | Reactivity Expected | Dilution info - | Notes - |
Transcriptional repressor which coordinates circadian rhythm and metabolic pathways in a heme-dependent manner. Integral component of the complex transcription machinery that governs circadian rhythmicity and forms a critical negative limb of the circadian clock by directly repressing the expression of core clock components BMAL1, CLOCK and CRY1. Also regulates genes involved in metabolic functions, including lipid and bile acid metabolism, adipogenesis, gluconeogenesis and the macrophage inflammatory response. Acts as a receptor for heme which stimulates its interaction with the NCOR1/HDAC3 corepressor complex, enhancing transcriptional repression. Recognizes two classes of DNA response elements within the promoter of its target genes and can bind to DNA as either monomers or homodimers, depending on the nature of the response element. Binds as a monomer to a response element composed of the consensus half-site motif 5'-[A/G]GGTCA-3' preceded by an A/T-rich 5' sequence (RevRE), or as a homodimer to a direct repeat of the core motif spaced by two nucleotides (RevDR-2). Acts as a potent competitive repressor of ROR alpha (RORA) function and regulates the levels of its ligand heme by repressing the expression of PPARGC1A, a potent inducer of heme synthesis. Regulates lipid metabolism by repressing the expression of APOC3 and by influencing the activity of sterol response element binding proteins (SREBPs); represses INSIG2 which interferes with the proteolytic activation of SREBPs which in turn govern the rhythmic expression of enzymes with key functions in sterol and fatty acid synthesis. Regulates gluconeogenesis via repression of G6PC1 and PEPCK and adipocyte differentiation via repression of PPARG. Regulates glucagon release in pancreatic alpha-cells via the AMPK-NAMPT-SIRT1 pathway and the proliferation, glucose-induced insulin secretion and expression of key lipogenic genes in pancreatic-beta cells. Positively regulates bile acid synthesis by increasing hepatic expression of CYP7A1 via repression of NR0B2 and NFIL3 which are negative regulators of CYP7A1. Modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy; controls mitochondrial biogenesis and respiration by interfering with the STK11-PRKAA1/2-SIRT1-PPARGC1A signaling pathway. Represses the expression of SERPINE1/PAI1, an important modulator of cardiovascular disease and the expression of inflammatory cytokines and chemokines in macrophages. Represses gene expression at a distance in macrophages by inhibiting the transcription of enhancer-derived RNAs (eRNAs). Plays a role in the circadian regulation of body temperature and negatively regulates thermogenic transcriptional programs in brown adipose tissue (BAT); imposes a circadian oscillation in BAT activity, increasing body temperature when awake and depressing thermogenesis during sleep. In concert with NR2E3, regulates transcriptional networks critical for photoreceptor development and function. In addition to its activity as a repressor, can also act as a transcriptional activator. In the ovarian granulosa cells acts as a transcriptional activator of STAR which plays a role in steroid biosynthesis. In collaboration with SP1, activates GJA1 transcription in a heme-independent manner. Represses the transcription of CYP2B10, CYP4A10 and CYP4A14 (By similarity). Represses the transcription of CES2 (By similarity). Represses and regulates the circadian expression of TSHB in a NCOR1-dependent manner (By similarity). Negatively regulates the protein stability of NR3C1 and influences the time-dependent subcellular distribution of NR3C1, thereby affecting its transcriptional regulatory activity (By similarity). Plays a critical role in the circadian control of neutrophilic inflammation in the lung; under resting, non-stress conditions, acts as a rhythmic repressor to limit inflammatory activity whereas in the presence of inflammatory triggers undergoes ubiquitin-mediated degradation thereby relieving inhibition of the inflammatory response (By similarity). Plays a key role in the circadian regulation of microglial activation and neuroinflammation; suppresses microglial activation through the NF-kappaB pathway in the central nervous system (By similarity). Plays a role in the regulation of the diurnal rhythms of lipid and protein metabolism in the skeletal muscle via transcriptional repression of genes controlling lipid and amino acid metabolism in the muscle (By similarity).
EAR1, HREV, THRAL, EAR1, HREV, THRAL, NR1D1, Nuclear receptor subfamily 1 group D member 1, Rev-erbA-alpha, V-erbA-related protein 1, EAR-1
Rabbit Recombinant Monoclonal NR1D1 antibody - conjugated to Alexa Fluor® 594.
IgG
Rabbit
Alexa Fluor® 594
Ex: 590nm, Em: 617nm
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 68% PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Liquid
Monoclonal
EPR10376
Affinity purification Protein A
Blue Ice
1-2 weeks
+4°C
-20°C
Upon delivery aliquot
Avoid freeze / thaw cycle, Store in the dark
This conjugated primary antibody is released using a quantitative quality control method that evaluates binding affinity post-conjugation and efficiency of antibody labeling.
For suitable applications and species reactivity, please refer to the unconjugated version of this clone. This conjugated antibody is eligible for the Abcam trial program.
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
This supplementary information is collated from multiple sources and compiled automatically.
NR1D1 also known as Rev-erbα is a nuclear receptor that plays an important role in the regulation of circadian rhythms and metabolism. It has an estimated mass of 68 kDa. This receptor functions as a transcriptional repressor and is responsible for binding to specific DNA sequences known as Rev-erb response elements (RREs). NR1D1 is well-expressed in various tissues with higher concentrations found in the liver muscle adipose tissue and brain. Its ability to repress gene expression is influenced by the presence of heme a ligand that binds to NR1D1 and modulates its activity.
NR1D1 regulates the expression of genes involved in the circadian clock and metabolic processes. It acts as part of a complex that includes co-repressors like NCoR and HDAC3 which helps modulate transcriptional repression. NR1D1 directly influences genes linked with lipid and glucose metabolism as well as inflammatory responses. By repressing the transcription of specific clock genes such as BMAL1 and CLOCK NR1D1 helps to maintain the body's internal clock synchronizing metabolic processes in accordance with the light-dark cycle.
The function of NR1D1 is integral in the circadian and metabolic pathways. It forms part of the feedback loop of the molecular circadian clock network working closely with proteins like PER and CRY to regulate circadian gene expression. In the metabolic pathway NR1D1 interacts with PPARγ and SREBP-1c orchestrating lipid homeostasis and energy balance. By integrating signals from the circadian system and the metabolic state of the organism NR1D1 ensures a harmonious coordination of these intricate biological processes.
NR1D1 has been implicated in metabolic disorders and sleep-related conditions. Disruptions in its function can lead to obesity and type 2 diabetes as NR1D1 affects key metabolic genes. It also has links to depression by influencing the circadian regulation of mood-controlling neurotransmitter systems. Research indicates that abnormalities in NR1D1 expression or function may negatively impact BMAL1 and other clock genes contributing to the pathogenesis of these conditions. Understanding the precise role of NR1D1 in these diseases could provide insights into new therapeutic strategies.
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This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
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