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Nature Neuroscience, ISSN 1097-6256, 2013, Volume 16, Issue 7, pp. 898 - 902
Journal Article
Nature Communications, ISSN 2041-1723, 11/2015, Volume 6, Issue 1, pp. 8893 - E5786
Journal Article
Journal Article
Molecular Cell, ISSN 1097-2765, 12/2013, Volume 52, Issue 6, pp. 769 - 782
Journal Article
Journal Article
Biochemical Journal, ISSN 0264-6021, 08/2014, Volume 461, Issue 3, pp. 477 - 486
HLCS (holocarboxylase synthetase) is a nuclear protein that catalyses the binding of biotin to distinct lysine residues in chromatin proteins. HLCS-dependent... 
Histone deacetylase 1 (HDAC1) | Epigenetics | Chromatin | Gene repression | Holocarboxylase synthetase (HLCS) | Nuclear receptor co-repressor (N-CoR) | gene repression | BIOTINYLATION | CELLS | METHYLATION | DROSOPHILA-MELANOGASTER | BIOCHEMISTRY & MOLECULAR BIOLOGY | N-COR | PATTERNS | chromatin | epigenetics | ELEMENTS | nuclear receptor co-repressor (N-CoR) | holocarboxylase synthetase (HLCS) | REGIONS | BIOTIN | EXPRESSION | histone deacetylase 1 (HDAC1) | Histone Deacetylase 1 - chemistry | Immunoprecipitation | Alternative Splicing | Epigenetic Repression | Humans | Nuclear Receptor Co-Repressor 1 - genetics | Genetic Complementation Test | Carbon-Nitrogen Ligases - genetics | Proteolysis | HEK293 Cells | Protein Interaction Domains and Motifs | Acetylation | Carbon-Nitrogen Ligases - chemistry | Histone Deacetylase 1 - genetics | Peptide Fragments - genetics | Biomarkers - metabolism | Recombinant Proteins - metabolism | Peptide Fragments - metabolism | Carbon-Nitrogen Ligases - metabolism | Nuclear Receptor Co-Repressor 1 - chemistry | Models, Molecular | Recombinant Proteins - chemistry | Mutant Proteins - metabolism | Peptide Fragments - chemistry | Mutant Proteins - chemistry | Nuclear Receptor Co-Repressor 1 - metabolism | Protein Processing, Post-Translational | Histones - metabolism | Amino Acid Substitution | Histone Deacetylase 1 - metabolism
Journal Article
Journal Article
Molecular Cell, ISSN 1097-2765, 05/2017, Volume 66, Issue 3, pp. 321 - 331.e6
The molecular mechanisms underlying the opposing functions of glucocorticoid receptors (GRs) and estrogen receptor α (ERα) in breast cancer development remain... 
nuclear receptors | transrepression | enhancers | transcriptional regulation | BREAST-CANCER | GENE REPRESSION | DNA-BINDING | NUCLEAR RECEPTORS | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR BINDING-SITES | DEPENDENT ENHANCER ACTIVATION | GENOME-WIDE ANALYSIS | ANTIINFLAMMATORY ACTIONS | COREGULATOR GRIP1 | ESTROGEN-RECEPTOR | CELL BIOLOGY | Transcription, Genetic - drug effects | Humans | Multiprotein Complexes | Transcriptome | Nuclear Receptor Co-Repressor 1 - genetics | Receptors, Glucocorticoid - metabolism | Breast Neoplasms - metabolism | Receptors, Glucocorticoid - agonists | Dexamethasone - pharmacology | Estrogen Receptor alpha - agonists | Transfection | MCF-7 Cells | RNA Interference | HEK293 Cells | Estrogen Receptor alpha - metabolism | Female | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | Estradiol - pharmacology | Histone Deacetylases - genetics | Nuclear Receptor Co-Repressor 2 - genetics | Signal Transduction | Down-Regulation | Histone Deacetylases - metabolism | Breast Neoplasms - genetics | Estrogen Receptor alpha - genetics | Enhancer Elements, Genetic | Breast Neoplasms - pathology | Nuclear Receptor Co-Repressor 1 - metabolism | Receptors, Glucocorticoid - genetics | Nuclear Receptor Co-Repressor 2 - metabolism | Protein Binding | Sumoylation | Mutation | Receptor Cross-Talk - drug effects
Journal Article
Cancer Research, ISSN 0008-5472, 11/2017, Volume 77, Issue 21, pp. 5808 - 5819
Journal Article
Journal Article
Nature communications, ISSN 2041-1723, 11/2018, Volume 9, Issue 1, pp. 4863 - 15
M2a-subtype macrophage activation is known to be impaired in obesity, although the underlying mechanisms remain poorly understood. Herein, we demonstrate that,... 
INFLAMMATION | MULTIDISCIPLINARY SCIENCES | RESISTANCE | IL-4 | KUPFFER CELLS | IKK-BETA | INSULIN-RECEPTOR SUBSTRATE-2 | MYELOID CELLS | HEPATIC STEATOSIS | POLARIZATION | ADIPOSE-TISSUE | Insulin Receptor Substrate Proteins - deficiency | Cell Proliferation | Coculture Techniques | Diet, High-Fat - adverse effects | Male | Nuclear Receptor Co-Repressor 1 - genetics | STAT6 Transcription Factor - genetics | Obesity - genetics | Proto-Oncogene Proteins c-akt - genetics | Hyperinsulinism - etiology | Receptor, Insulin - genetics | Hyperinsulinism - genetics | Obesity - etiology | Interleukin-4 - genetics | Insulin Receptor Substrate Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Hyperinsulinism - metabolism | Forkhead Box Protein O1 - metabolism | Histone Deacetylases - genetics | Macrophages - pathology | Signal Transduction | Interleukin-4 - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Insulin Resistance | Histone Deacetylases - metabolism | STAT6 Transcription Factor - metabolism | 3T3-L1 Cells | Macrophage Activation | Mice, Knockout | Obesity - metabolism | Obesity - pathology | Hyperinsulinism - pathology | Macrophages - metabolism | Animals | Nuclear Receptor Co-Repressor 1 - metabolism | Receptor, Insulin - metabolism | Mice | Forkhead Box Protein O1 - genetics | Cell Movement | Obesity | Hyperinsulinemia | Impairment | AKT protein | Activation | Macrophages | Insulin | Interleukin 4 | Cell activation | FOXO1 protein | Stat6 protein | Insulin resistance
Journal Article