Mammalian circadian rhythms are generated by a feedback loop in which BMAL1 and CLOCK, players of the positive limb, activate transcription of the cryptochrome and period genes, components of the negative limb. Bmal1 and Per transcription cycles display nearly opposite phases and are thus governed b …

The function of the nuclear receptor Rev-erbα (Nr1d1) in the brain is, apart from its role in the circadian clock mechanism, unknown. Therefore, we compared gene expression profiles in the brain between wild-type and Rev-erbα knock-out (KO) animals. We identified fatty acid binding protein 7 (Fabp7, Blbp) as a direct target of repression by REV-ERBα. Loss of Rev-erbα manifested in memory and mood related behavioral phenotypes and led to overexpression of Fabp7 in various brain areas including the subgranular zone (SGZ) of the hippocampus, where neuronal progenitor cells (NPCs) can initiate adult neurogenesis. We found increased proliferation of hippocampal neurons and loss of its diurnal pattern in Rev-erbα KO mice. In vitro, proliferation and migration of glioblastoma cells were affected by manipulating either Fabp7 expression or REV-ERBα activity. These results suggest an important role of Rev-erbα and Fabp7 in adult neurogenesis, which may open new avenues for treatment of gliomas as ...

TY - JOUR. T1 - Optimized chemical probes for REV-ERB alpha. AU - Trump, Ryan P.. AU - Bresciani, Stefano. AU - Cooper, Anthony W. J.. AU - Tellam, James P.. AU - Wojno, Justyna. AU - Blaikley, John. AU - Orband-Miller, Lisa A.. AU - Kashatus, Jennifer A.. AU - Boudjelal, Mohamed. AU - Dawson, Helen C.. AU - Loudon, Andrew. AU - Ray, David. AU - Grant, Daniel. AU - Farrow, Stuart N.. AU - Willson, Timothy M.. AU - Tomkinson, Nicholas C. O.. PY - 2013/6/13. Y1 - 2013/6/13. N2 - REV-ERB alpha has emerged as an important target for regulation of circadian rhythm and its associated physiology. Herein, we report on the optimization of a series of REV-ERB alpha agonists based on G5K4112 (1) for potency, selectivity, and bioavailability.(1) Potent REV-ERB alpha agonists 4, 10, 16, and 23 are detailed for their ability to suppress BMAL and IL-6 expression from human cells while also demonstrating excellent selectivity over LAR alpha. Amine 4 demonstrated in vivo bioavailability after either iv or oral ...

In liver, most metabolic pathways are under circadian control, and hundreds of protein-encoding genes are thus transcribed in a cyclic fashion. Here we show that rhythmic transcription extends to the locus specifying miR-122, a highly abundant, hepatocyte-specific microRNA. Genetic loss-of-function and gain-of-function experiments have identified the orphan nuclear receptor REV-ERBalpha as the major circadian regulator of mir-122 transcription. Although due to its long half-life mature miR-122 accumulates at nearly constant rates throughout the day, this miRNA is tightly associated with control mechanisms governing circadian gene expression. Thus, the knockdown of miR-122 expression via an antisense oligonucleotide (ASO) strategy resulted in the up- and down-regulation of hundreds of mRNAs, of which a disproportionately high fraction accumulates in a circadian fashion. miR-122 has previously been linked to the regulation of cholesterol and lipid metabolism. The transcripts associated w

Newswise - ST. LOUIS -. Saint Louis University researchers report in Molecular Metabolism new findings that the nuclear receptor REV-ERB appears to play a key role in muscle regeneration, suggesting the receptor may be a good target for new drugs to treat a variety of muscle disorders and injuries.. Colin Flaveny, Ph.D. assistant professor of pharmacology and physiology and Thomas Burris, Ph.D., chair of pharmacology and physiology at Saint Louis University, focus their work on identifying natural hormones that regulate nuclear receptors and then developing synthetic compounds to target these receptors in order to develop drugs to treat diseases.. Earlier this year, Burris published findings showing that a nuclear receptor called REV-ERB is involved in lowering LDL cholesterol. He previously studied REV-ERBs role in regulating mammals internal clocks.. Now teaming up, Flaveny and Burris are uncovering REV-ERBs role in muscle regeneration. REV-ERB is an interesting nuclear receptor that helps ...

Supplementary MaterialsSupplementary 1 41419_2019_1346_MOESM1_ESM. derive from autoregulatory and cell-autonomous tempo, which is produced by transcriptionCtranslation reviews loops3,4. Within this model, the heterodimeric transcriptional activators BMAL1 and CLOCK which contain bHLH and PAS domains promote the transcription of CACGTG E-box or E-box-like filled with clock-controlled genes (CCGs), such as for example Cryptochrome (Cry1-2) and Period (Per1-3) genes5C7. CRY and PER protein are synthesized within the cytoplasm and enter nucleus to bind and inhibit BMAL1: CLOCK heterodimers2,8,9. Besides, two nuclear receptors REV-ERB and ROR get excited about the BMAL1 transcription regulatory loops10C12. Posttranslational proteolysis and adjustments from the clock Anle138b protein get excited about the legislation of circadian clock1,13. The clock proteins enter nucleus to execute functions. Therefore the translocation between nucleus and cytoplasm is crucial in preserving the right speed from the ...

Dr. Mitchell Lazar is the Sylvan Eisman Professor of Medicine and Genetics, the Chief of the Division of Endocrinology, Diabetes, and Metabolism, and the Director of the Institute for Diabetes, Obesity, and Metabolism at the University of Pennsylvania.. Dr. Lazar received his undergraduate degree in Chemistry from the Massachusetts Institute of Technology, then received a PhD in Neurosciences and an MD from Stanford University. He trained in Internal Medicine at Brigham and Womens Hospital in Boston and in Endocrinology at the Massachusetts General Hospital before joining the University of Pennsylvania faculty in 1989.. Dr. Lazars research focus is on the epigenomic regulation of gene expression and metabolism. He is particularly interested in nuclear receptors, which are master regulators of metabolism. He discovered the heme receptor Rev-erbα and the epigenomic mechanisms by which it represses gene transcription to control circadian and metabolic physiology. He has also made seminal ...

The Lazar laboratory is studying the transcriptional regulation of metabolism. We are particularly focused on the role played by nuclear receptors (NRs). In the absence of ligand, NRs bind to DNA and function as potent transcriptional repressors by recruiting corepressor complexes that include the chromatin modulating enzyme histone deacetylase 3 (HDAC3). We are studying the tissue-specific and physiological roles of the corepressor complexes using by combining genomic, genetic, proteomic, bioinformatic, and metabolic phenotyping approaches. We are especially interested in the circadian NR Rev-erb alpha, which utilizes the corepressor complex to potently repress transcription. Rev-erb alpha is a key repressive component of the circadian clock that coordinates metabolism and biological rhythms. We are also studying PPAR gamma, a nuclear receptor that is a master regulator of adipocyte (fat cell) differentiation. Ligands for PPAR gamma have potent antidiabetic activity, and thus PPAR gamma ...

REV-ERB Agonist II, SR9009 - Calbiochem REV-ERB Agonist II, SR9009, CAS 1379686-30-2, acts as a specific REV-ERB-α/β agonist that exhibits a direct and reversible binding (Kd = 800 nM). - Find MSDS or SDS, a COA, data sheets and more information.

Nuclear receptor subfamily 1 group D member 2, BD73, V-erbA-related protein 1-related (EAR-1r), Hs.37288, HZF2, Rev-erb alpha-related receptor (RVR), Rev-erb-beta ...

Retinoic acid-related orphan receptors RORα and RORγ play a regulatory role in lipid/glucose homeostasis and various immune functions, and have been implicated in metabolic syndrome and several inflammatory diseases. RORα-deficient mice are protected against age- and diet-induced obesity, hepatosteatosis, and insulin resistance. The resistance to hepatosteatosis in RORα-deficient mice is related to the reduced expression of several genes regulating lipid synthesis, transport, and storage. Adipose tissue-associated inflammation, which plays a critical role in the development of insulin resistance, is considerably diminished in RORα-deficient mice as indicated by the reduced infiltration of M1 macrophages and decreased expression of many pro-inflammatory genes. Deficiency in RORγ also protects against diet-induced insulin resistance by a mechanism that appears different from that in RORα deficiency. Recent studies indicated that RORs provide an important link between the circadian clock machinery

Nfil3 expression is directly regulated by the core circadian clock transcriptional repressor REV-ERBα. In T cells and liver cells, REV-ERBα binds to a consensus sequence in the Nfil3 gene locus and represses transcription, resulting in a rhythmic diurnal Nfil3 expression pattern (6, 10). Rev-erbα transcript and protein abundance also oscillated diurnally in intestinal epithelial cells but was higher in germ-free mice versus conventional mice (Fig. 2, C and D). This suggested that REV-ERBα governs circadian rhythmicity in Nfil3 expression and that the microbiota might induce Nfil3 expression by repressing Rev-erbα expression. REV-ERBα bound directly to the Nfil3 promoter in intestinal epithelial cells, as assessed by chromatin immunoprecipitation (ChIP) assay (Fig. 2E). Further, Nfil3 expression in antibiotic-treated Rev-erbα−/− mice was similar to that in conventional wild-type mice (Fig. 2F). Thus, microbiota regulation of Nfil3 expression is REV-ERBα-dependent, and the microbiota ...

Nuclear Receptor Signaling (/Rhythmyx/assembler/render?sys_contentid=49860&sys_revision=1&sys_variantid=639&sys_context=0&sys_authtype=0&sys_siteid=&sys_folderid= sys_dependentvariantid=639 sys_dependentid=49860 inlinetype=rxhyperlink rxinlineslot=103 sys_dependentid=49860 sys_siteid= sys_folderid=) involves the study of the retinoic acid-related orphan receptors (ROR α-ϒ or NR1F1-3) and the orphan receptor TAK1 (TR4 or NR2C2). ...

Metabolic activities are regulated by the circadian clock, and disruption of the clock exacerbates metabolic diseases including obesity and diabetes. Transcriptomic studies in metabolic organs suggested that the circadian clock drives the circadian expression of important metabolic genes. Here we show that histone deacetylase 3 (HDAC3) is recruited to the mouse liver genome in a circadian manner. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Diurnal recruitment of HDAC3 corresponds to the expression pattern of REV-ERBα, an important component of the circadian clock. REV-ERBα colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbα in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by REV-ERBα directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis. In addition, we reported that the REV-ERBα paralog, REV-ERBβ also

CD8(+) T lymphocytes play a key role in host defense, in particular against important persistent viruses, although the critical functional properties of such cells in tissue are not fully defined. We have previously observed that CD8(+) T cells specific for tissue-localized viruses such as hepatitis C virus express high levels of the C-type lectin CD161. To explore the significance of this, we examined CD8(+)CD161(+) T cells in healthy donors and those with hepatitis C virus and defined a population of CD8(+) T cells with distinct homing and functional properties. These cells express high levels of CD161 and a pattern of molecules consistent with type 17 differentiation, including cytokines (e.g., IL-17, IL-22), transcription factors (e.g., retinoic acid-related orphan receptor gamma-t, P = 6 x 10(-9); RUNX2, P = 0.004), cytokine receptors (e.g., IL-23R, P = 2 x 10(-7); IL-18 receptor, P = 4 x 10(-6)), and chemokine receptors (e.g., CCR6, P = 3 x 10(-8); CXCR6, P = 3 x 10(-7); CCR2, P = 4 x 10(-7)).

Lam MT, Cho H, Lesch HP, Gosselin D, Heinz S, Tanaka-Oishi Y, Benner C, Kaikkonen MU, Kim AS, Kosaka M, Lee CY, Watt A, Grossman TR, Rosenfeld MG, Evans RM, Glass CK Rev-Erbs repress macrophage gene expression by inhibiting enhancer-directed transcription. Nature. 2013 Jun 27;498(7455):511-5. doi: 10.1038/nature12209. Epub 2013 Jun 2. PubMed PMID: 23728303; PubMed Central PMCID: PMC3839578.. Spann NJ, Garmire LX, McDonald JG, Myers DS, Milne SB, Shibata N, Reichart D, Fox JN, Shaked I, Heudobler D, Raetz CR, Wang EW, Kelly SL, Sullards MC, Murphy RC, Merrill AH Jr, Brown HA, Dennis EA, Li AC, Ley K, Tsimikas S, Fahy E, Subramaniam S, Quehenberger O, Russell DW, Glass CK. Regulated accumulation oF desmosterol integrates macrophage lipid metabolism and inflammatory responses. Cell. 2012 Sep 28;151(1):138-52. doi: 10.1016/j.cell.2012.06.054. PubMed PMID: 23021221; PubMed Central PMCID: PMC3464914.. Stender JD, Pascual G, Liu W, Kaikkonen MU, Do K, Spann NJ, Boutros M, Perrimon N, Rosenfeld MG, ...

PHILADELPHIA - A new appreciation for the interplay between two cell nucleus proteins that lead both intertwined and separate lives is helping researchers better understand fatty liver disease, according to a new study by researchers at the Perelman School of Medicine at the University of Pennsylvania. They published their findings this month in Genes & Development.. The liver normally makes and stores fat, which is required in moderation for normal body function. However, excess fat can cause major liver damage. In fact, fatty liver is a leading cause of liver failure in the United States and is often brought on by obesity and diabetes.. We showed that simply deleting the protein HNF6 in liver cells of adult transgenic mice fed normal laboratory chow leads to fatty liver syndrome, said senior author Mitchell Lazar, MD, PhD , director of the Institute Diabetes, Obesity, and Metabolism. Although HNF6 is known mainly as an activator of protein transcription, loss of it upregulates many ...

Electron microscopy analysis of muscle from Nr1d1−/− mice (with lower Rev-erbα) and WT (wild type, or normal) mice. Black arrows: swollen, less dense

NR1D1 or Rev-erb-alpha is so-called, because it is transcribed in the reverse direction and overlaps the 3 end of THRA, an important thyroid nuclear receptor. It is interesting that thyroid dysfunction becomes most prominent among bipolar patients after treatment with lithium [46]. Also, thyroid (T3) augmentation is useful for treating depression [47]. Thyroid has been used for periodic catatonia (perhaps a form of bipolar disorder) since the 1930s [1]. Considering that the intronic location of rs2314339 indicates no obvious functional role, we suspect that this SNP might be in linkage disequilibrium with some nearby polymorphism with a key functional effect. As linkage disequilibrium for rs2314339 extends through most of NR1D1 and to the 3 end of THRA, the functional element could plausibly be situated in either gene.. A coding SNP in PPARGC1B, Pro203Ala, rs7732671, was over-transmitted to bipolar probands with P , 0.05 and odds ratio 1.55. By itself, we might regard this isolated finding as ...

In February, the company announced it would acquire the US and Canadian rights to Actavis branded respiratory drug business for an initial sum of $600 million.[41] Later in the same month the company announced it would partner with Orca Pharmaceuticals to develop retinoic acid-related orphan nuclear receptor gamma inhibitors for use in the treatment of a number of autoimmune diseases, which could generate up to $122.5 million for Orca.[42] The company also announced their plan to spend $40 million creating a new subsidiary focused on small molecule anti-infectives - primarily in the research of the gyrase inhibitor, AZD0914, which is currently in Phase II for the treatment of gonorrhea.[43] The company underwrote twenty out of thirty-two seats of a new Cambridge-Gothenburg service by Sun-Air of Scandinavia.[44]. In mid-March the company announced it would co commercialise naloxegol along with Daiichi Sankyo in a deal worth up to $825 million.[45] Towards the end of April the company announced a ...

The discovery of increasing numbers of genes with overlapping sequences highlights the problem of expression in the context of constraining regulatory elements from more than one gene. This study identifies regulatory sequences encompassed within two genes that overlap in an antisense orientation at their 3 ends. The genes encode the α-thyroid hormone receptor gene (TRα or NR1A1) and Rev-erbα (NR1D1). In mammals TRα pre-mRNAs are alternatively spliced to yield mRNAs encoding functionally antagonistic proteins: TRα1, an authentic thyroid hormone receptor; and TRα2, a non-hormone-binding variant that acts as a repressor. TRα2-specific splicing requires two regulatory elements that overlap with Rev-erbα sequences. Functional mapping of these elements reveals minimal splicing enhancer elements that have evolved within the constraints of the overlapping Rev-erbα sequence. These results provide insight into the evolution of regulatory elements within the context of bidirectional coding sequences.

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The mechanism of LPS-stimulated HIF1α induction involves succinate, which inhibits prolyl hydroxylases (PHDs). Pyruvate kinase M2 (PKM2) is also induced and interacts with and promotes the function of HIF1α. In another critical inflammatory cell type, Th17 cells, HIF1α acts via the retinoic acid-related orphan receptor-γt (RORγt) to drive Th17 differentiation. HIF1α is therefore a key reprogrammer of metabolism in inflammatory cells that promotes inflammatory gene expression.. ...

The mechanism of LPS-stimulated HIF1α induction involves succinate, which inhibits prolyl hydroxylases (PHDs). Pyruvate kinase M2 (PKM2) is also induced and interacts with and promotes the function of HIF1α. In another critical inflammatory cell type, Th17 cells, HIF1α acts via the retinoic acid-related orphan receptor-γt (RORγt) to drive Th17 differentiation. HIF1α is therefore a key reprogrammer of metabolism in inflammatory cells that promotes inflammatory gene expression.. ...

Both epidemiological and clinical data suggest circadian involvement in the predisposition, etiology, and progression of immune-related morbidities, such as cancer and autoimmune diseases (37, 38). Inflammatory diseases, in particular, exhibit strong time-of-day symptoms. For example, rheumatoid arthritis has a strong diurnal variation in disease expression, which is accompanied by fluctuations in circulating IL-6 concentration (39). LPS-induced endotoxin shock displays temporal dependency (40), and circadian disruption mimicking jet lag can greatly magnify LPS response (41). According to recent evidence, components of the circadian clock regulate the expression of innate immune molecules, such as proinflammatory cytokines (42) and pattern recognition receptors (14). Rev-erbα is a key clock gene that controls inflammatory cytokine genes, including Il6, in macrophages, indicating that it negatively regulates the inflammatory responses in macrophages (11). In the current study, we found that ...

SR9009, also known as Stenabolic, is a research drug that was developed by professor Thomas Burris of the Scripps Research Institute as an agonist of Rev-ErbA (i.e., increases the constitutive repression of genes regulated by Rev-ErbA)[1] with a half-maximum inhibitory concentration (IC50) = 670 nM for Rev-ErbAα and IC50 = 800 nM for Rev-ErbAβ.[2] Activation of Rev-ErbA-α by SR9009 in mice increases exercise capacity by increasing mitochondria counts in skeletal muscle.[3] Abuse of SR9009 has been reported within the bodybuilding community, resulting in SR9009 being placed on the World Anti-Doping Agency list of prohibited drugs. SR9009 and the related SR9011 drug are described as Hormone and Metabolic Modulators.[4][5] ...

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A 2/N mode dock generator that generates bus clock signals through the use of bus clock enable signals selecting bus clock pulses that are in phase and out of phase with a core clock signal. The clock generator maintains synchronization between the bus clock signal and the core clock signal so that they are always in a predetermined phase relationship.

cdna: chromosome:VEGA66:4:133553376:133556536:1 gene:OTTMUSG00000011155 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Nr0b2 description:nuclear receptor subfamily 0, group B, member 2 ...

SR9011 Description:. SR9011 is a trifunctional methacrylate monomer that provides exceptional adhesion to metal substrates.. SR9011 is recommended for use in peroxide cured coatings, sealants, and PVC-based plastisols. Usage levels of 5% to 10% by weight are recommended.. SR9011 is a potent and specific synthetic REV-ERB. It also has good in vivo plasma/brain exposure. The nuclear receptors REV-ERB-α and REV-ERB-β play an integral role in regulating the expression of core clock proteins, driving rhythms in activity and metabolism. Administration of SR9011 alters circadian behavior and the circadian pattern of core clock gene expression in the hypothalami of mice. The circadian expression pattern of an array of metabolic genes in the liver, skeletal muscle and adipose tissue was also altered, resulting in increased energy expenditure. Treatment of diet-induced obese mice with SR9011 decreased obesity by reducing fat mass and markedly improved dyslipidaemia and hyperglycaemia. These results ...

Colin Flaveny, Ph.D. pal with professor of pharmacology and physiology and Thomas Burris, Ph.D., point the way of pharmacology and physiology at Saint Louis University, unenlightened their sedulity on identifying innate hormones that carry on nuclear receptors and then picketing synthetic paratheses to butt these receptors in systematize to age poisons to upon maladies.. Earlier this year, Burris let oned findings be identifiable that a atomic receptor wailed REV-ERB is charged in lowering LDL cholesterol. He yesterday deliberate REV-ERBs guilt in regulating mammals internal clocks.. Now join forcing up, Flaveny and Burris are uncovering REV-ERBs locus in muscle regeneration.. REV-ERB is an charming nuclear receptor that lifts coordinating our metabolism with our day after day ordinary, Flaveny conveyed. Were studying the protein to see if accoutring its undertaking up or down can instigate the way muscle regenerates after mistreat or illness.. Skeletal muscle comprises 40 to 50 percent ...

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The recurrent missense variant in Nuclear Receptor Subfamily 2 Group E Member 3 (NR2E3), c.166G>A, p.(Gly56Arg) or G56R, underlies 1%-2% of cases with ...

I think if you ever wanted to know what gene expression exactly is, look no further than nuclear receptors. You have receptors around your DNA nucleus in your cells that bind different things, this basically causes activation of your DNA to produce difference proteins ( polypeptides is a better word ) , thus expressing different genes ...

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TY - JOUR. T1 - Adrenergic regulation of clock gene expression in mouse liver. AU - Terazono, Hideyuki. AU - Mutoh, Tatsushi. AU - Yamaguchi, Shun. AU - Kobayashi, Masaki. AU - Akiyama, Masashi. AU - Udo, Rhyuta. AU - Ohdo, Shigehiro. AU - Okamura, Hitoshi. AU - Shibata, Shigenobu. N1 - Copyright: Copyright 2008 Elsevier B.V., All rights reserved.. PY - 2003/5/27. Y1 - 2003/5/27. N2 - A main oscillator in the suprachiasmatic nucleus (SCN) conveys circadian information to the peripheral clock systems for the regulation of fundamental physiological functions. Although polysynaptic autonomic neural pathways between the SCN and the liver were observed in rats, whether activation of the sympathetic nervous system entrains clock gene expression in the liver has yet to be understood. To assess sympathetic innervation from the SCN to liver tissue, we investigated whether injection of adrenaline/ noradrenaline (epinephrine/norepinephrine) or sympathetic nerve stimulation could induce mPer gene expression ...

U2OS cells harbor a circadian clock but express only a few rhythmic genes in constant conditions. We identified 3040 binding sites of the circadian regulators BMAL1, CLOCK and CRY1 in the U2OS genome. Most binding sites even in promoters do not correlate with detectable rhythmic transcript levels. Luciferase fusions reveal that the circadian clock supports robust but low amplitude transcription rhythms of representative promoters. However, rhythmic transcription of these potentially clock-controlled genes is masked by non-circadian transcription that overwrites the weaker contribution of the clock in constant conditions. Our data suggest that U2OS cells harbor an intrinsically rather weak circadian oscillator. The oscillator has the potential to regulate a large number of genes. The contribution of circadian versus non-circadian transcription is dependent on the metabolic state of the cell and may determine the apparent complexity of the circadian transcriptome. Hoffmann, Julia; Symul, Laura; Shostak,

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Author: Nakamura, Y. et al.; Genre: Journal Article; Published online: 2014-07; Title: Diurnal and circadian expression profiles of glycerolipid biosynthetic genes in Arabidopsis

Circadian clock gene expression in in vitro cultured CD4+ T cells and PER2::Luciferase CD4+ reporter T cells. Blood was sampled from 3 nutritious younger males

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