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Extensive characterization of NF-kappaB binding uncovers non-canonical motifs and advances the interpretation of genetic functional traits

ABSTRACT: We report the DNA binding preferences of 4 NF-kappaB dimers (p52p52, RELARELA, RELAp50, RELAp52)

ORGANISM(S): Homo sapiens

PROVIDER: GSE29460 | GEO | 2011/05/24

SECONDARY ACCESSION(S): PRJNA141581

REPOSITORIES: GEO

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Extensive characterization of NF-kappaB binding uncovers non-canonical motifs and advances the interpretation of genetic functional traits

Project description:We report the DNA binding preferences of 4 NF-kappaB dimers (p52p52, RELARELA, RELAp50, RELAp52) Proteins of the Nf-kappab family were bound to DNA oligonucleotides containing a degenerate region. The protein-DNA complexes were selected after one or multiple rounds of SELEX and the DNA molecules were deep sequenced.

2011-05-24 | E-GEOD-29460 | biostudies-arrayexpress

Extensive characterization of NF-?B binding uncovers non-canonical motifs and advances the interpretation of genetic functional traits.

Project description: Not available

| S-EPMC3218832 | biostudies-literature

RelA Nuclear factor-kappaB (NF-kB) Subunit binding Loci in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells (Promoter)

Project description:A study to define the binding loci of RelA-containing NF-kappaB dimers in a human myometrial smooth muscle cell line after exposure to TNF.

2015-03-31 | GSE65690 | GEO

RelA Nuclear factor-kappaB (NF-kB) Subunit binding Loci in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells (expression)

2015-03-31 | GSE65707 | GEO

Suppression of p53-mediated senescence by non-canonical NF-kappaB pathway mediated regulation of EZH2 expression

Project description:The NF-kappaB and p53 transcription factors control the expression of complex gene regulatory networks in response to many cell stresses and stimuli. This experiment describes gene expression profiling of cells depleted for EZH2, NF-kappaB2, RelB and p53. We find that EZH2 is the major effector of crosstalk between the alternative NF-kappaB and p53 pathways and acts to suppress cellular senescence. Total RNA was obtained from primary juvenile human dermal fibroblasts 48 hours after transfection with siRNA specific for one, or a targeted combination of the transcription factors, or a scrambled siRNA control.

2014-03-31 | E-MTAB-1593 | biostudies-arrayexpress

RelA Nuclear factor-kappaB (NF-kB) Subunit binding Loci in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells (expression)

Project description:A study to define the binding loci of RelA-containing NF-kappaB dimers and subsequent correlation with gene expression in a human myometrial smooth muscle cell line after exposure to TNF. Monolayers of PHM1-31 cells were exposed to TNF (10ng/ml) for 1 hour or left unstimulated. Total RNA was isolated, prepared and used to probe AffymetrixU133Plus2 expression arrays. Both datasets were subsequently analysed in Partek Genomics Suite V6.6 and correlations between promoter occupancy (promoter arrays) and gene expression (expression arrays) were made.

2015-03-31 | E-GEOD-65707 | biostudies-arrayexpress

RelA Nuclear factor-kappaB (NF-kB) Subunit binding Loci in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells (Promoter)

Project description:A study to define the binding loci of RelA-containing NF-kappaB dimers in a human myometrial smooth muscle cell line after exposure to TNF. Monolayers of PHM1-31 cells were exposed to TNF (10ng/ml) for 1 hour or left unstimulated. The Chromatin immunoprecipitation (ChIP) assay was performed to recover RelA-bound chromatin or non-specifically bound chromatin with IgG. That chromatin was prepared and used to probe Affymetrix GeneChIP 1.0R Human Promoter arrays. Three biological replicates of each experiment were conducted. Datasets were subsequently analysed in Partek Genomics Suite V6.6 where baseline was normalised by subtraction of IgG values from conrresponding RelA-immunoprecipitated samples. Control samples immunoprecipitated with RelA were then compared with TNF-stimulated samples immunoprecipitated with RelA.

2015-03-31 | E-GEOD-65690 | biostudies-arrayexpress

Transgenic inhibition of astroglial NF-kappaB in experimental autoimmune encephalomyelitis

Project description:In the central nervous system (CNS) the transcription factor NF-kappaB is a key regulator of inflammation and secondary injury processes. Following trauma or disease, the expression of NF-kappaB-dependent genes is activated, leading to both protective and detrimental effects on CNS recovery. Here we show that transgenic inactivation of astroglial NF-kappaB in mice (GFAP-IkappaBalpha-dn mice) resulted in dramatic reduction of disease severity and improvement in functional recovery following EAE. This coincided with a higher presence of leukocytes in the cord and brain of transgenic mice at the chronic phase of the disease, when the functional recovery over WT mice was the most significant. We observed that expression of proinflammatory genes in both spinal cord and cerebellum was delayed and reduced, while the loss of neuronal-specific molecules essential for synaptic transmission was limited compared to WT mice. Furthermore, death of retinal ganglion cells in affected retinas was almost abolished, suggesting the activation of neuroprotective mechanisms. Our data indicate that inhibiting NF-kappaB in astrocytes results in neuroprotective effects following EAE, directly implicating astrocytes in the pathophysiology of this disease. Keywords: time course, EAE, transgenic mice, astrocytes, inflammation, cytokines, chemokines

2009-01-01 | GSE10235 | GEO

Human variation in PolII and NF-KappaB binding (ChIP-seq study with NF-KappaB)

Project description:We examined genome-wide variation in transcription factor binding in different individuals and a chimpanzee using chromatin immunoprecipitation followed by massively-parallel sequencing (ChIP-Seq). The binding sites of RNA Polymerase II (Pol II) as well as a key regulator of immune responses, NFkB, were mapped in ten HapMap lymphoblastoid cell lines derived from individuals of African, European, and Asian ancestry, including a parent-offspring trio. We also mapped gene expression in all ten human cell lines for two treatment conditions: a) no treatment and b) following induction by TNF-alpha. Genome-wide comparison of Pol II and NF-KappaB binding in ten individuals. ChIP-seq with NF-KappaB.

2010-03-22 | E-GEOD-19485 | biostudies-arrayexpress

Tumor suppression via inhibition of SWI/SNF complex-dependent NF-kappaB activation [A549 subset]

Project description:The transcription factor NF-kappaB is constitutively activated in many epithelial tumors but few NF-kappaB inhibitors are suitable for cancer therapy because of the broad biological effects of NF-κB. We previously reported that the d4 family (DPF1, DPF2, DPF3a/b) function as adaptor proteins linking NF-kappaB with the SWI/SNF complex. Here, we demonstrate that in epithelial tumor cell lines, exogenous expression of the highly conserved N-terminal 84-amino acid region of either DPF2 or DPF3a/b (designated “CT1”) has stronger inhibitory effects on anchorage-independent growth than single knockdown of any d4 protein, indicating that CT1 can function as an efficient dominant-negative mutant of the entire d4 family. By proximity ligation assays, CT1 was further shown to retain full function as an adaptor. Microarray analysis categorized NF-kappaB target genes by their CT1 sensitivity. Among CT1-sensitive genes, IL-6 was shown to strongly contribute to the anchorage-independent growth. Finally, exogenous CT1 expression efficiently suppressed tumor formation in a mouse xenograft model, suggesting that the d4 protein family could be a promising cancer therapy target.

2017-09-22 | GSE93768 | GEO

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