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Nature Reviews Drug Discovery, ISSN 1474-1776, 2014, Volume 13, Issue 3, pp. 197 - 216
The nuclear receptors REV-ERB (consisting of REV-ERB alpha and REV-ERB beta) and retinoic acid receptor-related orphan receptors (RORs; consisting of ROR... 
KAPPA-B ACTIVATION | RETINOIC ACID | PERIPHERAL CIRCADIAN CLOCKS | SKELETAL-MUSCLE CELLS | URSOLIC ACID PROMOTES | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | X-RAY-STRUCTURE | GENE-EXPRESSION | ORPHAN RECEPTOR | PHARMACOLOGY & PHARMACY | LIGAND-BINDING DOMAIN | T(H)17 CELL-DIFFERENTIATION | Neoplasms - metabolism | Nuclear Receptor Subfamily 1, Group D, Member 1 - chemistry | Humans | Receptors, Retinoic Acid - chemistry | Nuclear Receptor Subfamily 1, Group D, Member 1 - antagonists & inhibitors | Nuclear Receptor Subfamily 1, Group F, Member 1 - metabolism | Receptors, Cytoplasmic and Nuclear - chemistry | Nuclear Receptor Subfamily 1, Group D, Member 1 - metabolism | Nuclear Receptor Subfamily 1, Group F, Member 1 - chemistry | Atherosclerosis - drug therapy | Diabetes Mellitus - drug therapy | Diabetes Mellitus - metabolism | Receptors, Retinoic Acid - antagonists & inhibitors | Receptors, Retinoic Acid - metabolism | Nuclear Receptor Subfamily 1, Group F, Member 1 - antagonists & inhibitors | Atherosclerosis - metabolism | Neoplasms - drug therapy | Animals | Signal Transduction - drug effects | Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors | Ligands | Signal Transduction - physiology | Drug Delivery Systems - trends | Drug Delivery Systems - methods | Receptors, Cytoplasmic and Nuclear - metabolism | Drug targeting | Cell receptors | Pharmacology, Experimental | Research | Properties
Journal Article
Immunity, ISSN 1074-7613, 04/2014, Volume 40, Issue 4, pp. 477 - 489
We identified three retinoid-related orphan receptor gamma t (RORγt)-specific inhibitors that suppress T helper 17 (Th17) cell responses, including... 
PATHWAYS | TARGET GENES | FOXP3 OCCUPANCY | T(H)17 | REGULATORY NETWORK | RECEPTOR | DIFFERENTIATION | IMMUNOLOGY | PSORIASIS | ANTI-INTERLEUKIN-17 MONOCLONAL-ANTIBODY | TH17 CELLS | Myelin-Oligodendrocyte Glycoprotein - immunology | T-Lymphocyte Subsets - immunology | Transcription, Genetic - drug effects | Nuclear Receptor Subfamily 1, Group F, Member 3 - antagonists & inhibitors | Humans | Transcriptional Activation - drug effects | Encephalomyelitis, Autoimmune, Experimental - immunology | Structure-Activity Relationship | Gene Regulatory Networks - drug effects | Cell Lineage - drug effects | Systems Biology | Benzhydryl Compounds - chemistry | Heterocyclic Compounds, 4 or More Rings - pharmacology | Th17 Cells - drug effects | T-Lymphocyte Subsets - drug effects | Peptide Fragments - immunology | Protein Binding - drug effects | Benzeneacetamides - chemistry | Benzeneacetamides - pharmacology | Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | Cytokines - metabolism | Encephalomyelitis, Autoimmune, Experimental - drug therapy | Mice, Inbred C57BL | Heterocyclic Compounds, 4 or More Rings - chemistry | Digoxin - chemistry | Digoxin - pharmacology | Mice, Knockout | Animals | Androstenols - chemistry | Cell Differentiation - drug effects | Cell Line, Tumor | Multiple Sclerosis - immunology | Th17 Cells - immunology | Benzhydryl Compounds - pharmacology | Mice | Multiple Sclerosis - drug therapy
Journal Article
Nature, ISSN 0028-0836, 05/2012, Volume 485, Issue 7396, pp. 62 - 68
Journal Article
Journal Article
Cell Metabolism, ISSN 1550-4131, 12/2015, Volume 22, Issue 6, pp. 1009 - 1019
The oncogene encodes MYC, a transcription factor that binds the genome through sites termed E-boxes (5′-CACGTG-3′), which are identical to the binding sites of... 
GENE | COPY NUMBER | TRANSCRIPTION | ENDOCRINOLOGY & METABOLISM | N-MYC | C-MYC | REV-ERB-ALPHA | NEUROBLASTOMA | OVARIAN-CANCER | DIFFERENTIATION | EXPRESSION | CELL BIOLOGY | Humans | CLOCK Proteins - chemistry | Glutamine - metabolism | CLOCK Proteins - genetics | RNA, Messenger - metabolism | Nuclear Receptor Subfamily 1, Group D, Member 1 - antagonists & inhibitors | Repressor Proteins - antagonists & inhibitors | CLOCK Proteins - metabolism | Period Circadian Proteins - genetics | RNA Interference | Base Sequence | Binding Sites | Dimerization | Nuclear Receptor Subfamily 1, Group D, Member 1 - metabolism | Genes, Reporter | Repressor Proteins - metabolism | Promoter Regions, Genetic | ARNTL Transcription Factors - genetics | Nuclear Receptor Subfamily 1, Group D, Member 1 - genetics | ARNTL Transcription Factors - metabolism | Repressor Proteins - genetics | Receptors, Cytoplasmic and Nuclear - genetics | Circadian Rhythm | Proto-Oncogene Proteins c-myc - metabolism | Period Circadian Proteins - metabolism | Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors | ARNTL Transcription Factors - chemistry | Cell Line, Tumor | Glucose - metabolism | Proto-Oncogene Proteins c-myc - genetics | RNA, Small Interfering - metabolism | Receptors, Cytoplasmic and Nuclear - metabolism | Glucose metabolism | Medical colleges | Genomics | Cancer cells | Physiological aspects | Glucose | Dextrose | Cancer | Resveratrol
Journal Article
Nucleic Acids Research, ISSN 0305-1048, 09/2012, Volume 40, Issue 17, pp. 8519 - 8535
In this study, we demonstrate that the lack of retinoic acid-related orphan receptor (ROR) gamma or alpha expression in mice significantly reduced the peak... 
STAGGERER | METABOLISM | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | PROFILING REVEALS | REV-ERB-ALPHA | DEFICIENT MICE | DIFFERENTIATION | HISTONE ACETYLATION | ORPHAN NUCLEAR RECEPTOR | BETA | Cell Line | Chromatin - metabolism | Nuclear Receptor Subfamily 1, Group F, Member 3 - antagonists & inhibitors | Response Elements | Transcriptional Activation | Circadian Rhythm - genetics | Circadian Rhythm Signaling Peptides and Proteins - genetics | Gene Expression Regulation | ARNTL Transcription Factors - metabolism | Circadian Rhythm Signaling Peptides and Proteins - biosynthesis | Mice, Neurologic Mutants | Mice, Knockout | Nuclear Receptor Subfamily 1, Group F, Member 1 - metabolism | CLOCK Proteins - metabolism | Animals | Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism | Mice | Nuclear Receptor Subfamily 1, Group F, Member 1 - genetics | Nuclear Receptor Subfamily 1, Group D, Member 1 - metabolism | Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | Chromatin - chemistry | Cryptochromes - metabolism | Circadian rhythms | Chromatin | Transcription | Gene regulation | Liver | Regulatory sequences | CLOCK protein | Orphan receptors | Polymerase chain reaction | Reporter gene | Transcription activation | BMAL1 protein | Cryptochromes | Histones | Acetylation | Period 2 protein | Molecular Biology
Journal Article