Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response. - Wikidata - wikimedia - TriplyDB

Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response.

Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response.

http://www.wikidata.org/entity/Q41193370

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Epigenetic Control of Macrophage Polarisation and Soluble Mediator Gene Expression during Inflammation Molecular control of activation and priming in macrophages Exploiting genomics and natural genetic variation to decode macrophage enhancers Chemokines and microRNAs in atherosclerosis Towards an understanding of cell-specific functions of signal-dependent transcription factors Mechanisms Underlying the Selection and Function of Macrophage-Specific Enhancers Macrophages: gatekeepers of tissue integrity The selection and function of cell type-specific enhancers Reprogramming of lysosomal gene expression by interleukin-4 and Stat6 Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription The IL-4/STAT6 signaling axis establishes a conserved microRNA signature in human and mouse macrophages regulating cell survival via miR-342-3p CCDC88B is a novel regulator of maturation and effector functions of T cells during pathological inflammation Thyroid hormone receptor repression is linked to type I pneumocyte-associated respiratory distress syndrome A negative feedback loop mediated by the Bcl6-cullin 3 complex limits Tfh cell differentiation Cistrome plasticity and mechanisms of cistrome reprogramming Large-scale quality analysis of published ChIP-seq data.Neuroprotective pentapeptide CN-105 is associated with reduced sterile inflammation and improved functional outcomes in a traumatic brain injury murine model.MKL1 defines the H3K4Me3 landscape for NF-κB dependent inflammatory response.Deficiency of the transcriptional repressor B cell lymphoma 6 (Bcl6) is accompanied by dysregulated lipid metabolism Disruption of mammalian target of rapamycin complex 1 in macrophages decreases chemokine gene expression and atherosclerosis.Copper metabolism domain-containing 1 represses genes that promote inflammation and protects mice from colitis and colitis-associated cancer The active enhancer network operated by liganded RXR supports angiogenic activity in macrophages.An integrated ChIP-seq analysis platform with customizable workflows Extensive remodeling of DC function by rapid maturation-induced transcriptional silencing.Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.Reciprocal occupancy of BCL6 and STAT5 on Growth Hormone target genes: contrasting transcriptional outcomes and promoter-specific roles of p300 and HDAC3.MicroRNAs Control Macrophage Formation and Activation: The Inflammatory Link between Obesity and Cardiovascular Diseases Epigenomics of macrophages.Combined ChIP-Seq and transcriptome analysis identifies AP-1/JunD as a primary regulator of oxidative stress and IL-1β synthesis in macrophages.Molecular mechanisms that influence the macrophage m1-m2 polarization balance.Inflammation-sensitive super enhancers form domains of coordinately regulated enhancer RNAs.Macrophage polarization phenotype regulates adiponectin receptor expression and adiponectin anti-inflammatory response.Expression and regulation of long noncoding RNAs in TLR4 signaling in mouse macrophages BTB-ZF transcriptional regulator PLZF modifies chromatin to restrain inflammatory signaling programs.Ligand binding shifts highly mobile retinoid X receptor to the chromatin-bound state in a coactivator-dependent manner, as revealed by single-cell imaging.C26 cancer-induced muscle wasting is IKKβ-dependent and NF-kappaB-independent.Application of ChIP-Seq and related techniques to the study of immune function.The KRAB zinc finger protein ZFP809 is required to initiate epigenetic silencing of endogenous retroviruses.Dynamic expression of BCL6 in murine conventional dendritic cells during in vivo development and activation.Sulfonation pathway inhibitors block reactivation of latent HIV-1.

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P2860

Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response.

http://www.wikidata.org/entity/Q41193370

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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2010年论文

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2010年论文

@zh-cn

name

Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response.

@en

type

label

Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response.

@en

prefLabel

Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response.

@en

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P1433

Genes & Development

P1476

Bcl-6 and NF-kappaB cistromes mediate opposing regulation of the innate immune response

@en

P2093

Alexander L Dent

http://www.w3.org/2001/XMLSchema#string

Corinne B Ocampo

http://www.w3.org/2001/XMLSchema#string

Grant D Barish

http://www.w3.org/2001/XMLSchema#string

Jesse Dixon

http://www.w3.org/2001/XMLSchema#string

Malith Karunasiri

http://www.w3.org/2001/XMLSchema#string

Rajendra K Tangirala

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Ruth T Yu

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P2860

BCoR, a novel corepressor involved in BCL-6 repression

Class II histone deacetylases are directly recruited by BCL6 transcriptional repressor

Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identities

Pattern recognition receptors and inflammation

Distinct and predictive chromatin signatures of transcriptional promoters and enhancers in the human genome

Transcriptional repression of atherogenic inflammation: modulation by PPARdelta

ChIP-seq accurately predicts tissue-specific activity of enhancers

Bcl6 is a transcriptional repressor for the IL-18 gene

Cooperative NCoR/SMRT interactions establish a corepressor-based strategy for integration of inflammatory and anti-inflammatory signaling pathways

The BCL-6 proto-oncogene controls germinal-centre formation and Th2-type inflammation

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2760-2765

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scholarly article

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10.1101/GAD.1998010

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24

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24

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Ronald M. Evans

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2010-11-24T00:00:00Z

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49634902

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21106671

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3003193

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