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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65707 | GEO | 2015/03/31

SECONDARY ACCESSION(S): PRJNA274789

REPOSITORIES: GEO

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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 (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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-03-31 | GSE65721 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-03-31 | E-GEOD-65721 | biostudies-arrayexpress

Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

Project description:Using a mouse model with hepatocyte-specific deletion of transcription factor NF-κB RelA (p65), our group has previously revealed the important role of RelA in inducing the acute phase response, maintaining host defense, and preventing liver injury during sepsis. To goal of this study was determine the influence of RelA on hepatic gene changes that provide liver protection during infection. Mice were generated with functional deletion of NF-kappaB RelA (p56) in hepatocytes using a Cre-LoxP system. Mutant mice expressed Cre-recombinase under the transcriptional control of an albumin promotor and homozygous floxed RelA alleles. Wild type control mice lack the Cre-recombinase. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal bacteremia.

2019-06-07 | GSE126642 | GEO

Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of NF-kappaB RelA (p65) on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of NF-kappaB RelA (p65) in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.

2012-02-16 | GSE35513 | GEO

The RelA T505A mouse reveals important NF-kappaB regulatory pathways controlling cell proliferation, apoptosis and lymphomagenesis

Project description:Phosphorylation of the RelA(p65) Thr505 residue by Chk1 provides a mechanism of crosstalk between NF-kappaB signalling and DNA replication stress but its physiological significance was not known. Therefore, to learn more about the role of this pathway in vivo, we generated a knockin mouse with a RelA T505A mutation. Unlike RelA knockout mice, the RelA T505A mice develop normally but exhibit a variety of aberrant responses to stress. Following partial hepatectomy, livers from RelA T505A mice proliferate more rapidly. Moreover, in the Emu-Myc B-cell lymphoma model, tumorigenesis is more rapid and mice succumb to disease at significantly earlier times. Analysis of embryonic fibroblasts from RelA T505A mice challenged with a range of DNA damaging agents revealed loss of pro-apoptotic RelA functions, at least in part due to DUSP1 dependent regulation of p38 MAP kinase activity. This data reveals a critical pathway controlling NF-kappaB function that acts to suppress tumour-promoting activities of RelA.

2015-11-30 | E-MTAB-2686 | biostudies-arrayexpress

Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

Project description:Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

| PRJNA522786 | ENA

Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia

2012-02-16 | E-GEOD-35513 | biostudies-arrayexpress