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The NFkB protein RELA/p65 binds predominantly transcript introns and exons

ABSTRACT: We investigated the ability of the NFkB protein p65 to bind RNA and what its target transcrips were. In this CLIP-seq experiment we demonstrated that p65 is capable of binding RNA and it has a preference to introns and exons, suggesting it binds unspliced RNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE197705 | GEO | 2022/03/08

REPOSITORIES: GEO

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The NFkB protein RELA/p65 binds predominantly transcript introns and exons

Project description:The NFkB protein RELA/p65 binds predominantly transcript introns and exons

| PRJNA811611 | ENA

Myeloid cell RelA/p65 promotes lung cancer proliferation

Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array Analysis of gene expression in lewis lung carcinoma cells resected from lungs of WT and RelA/p65 deficient mice exposed to smoke or air. Four different samples were analyzed (3 replicates each).

2012-03-31 | E-GEOD-36568 | biostudies-arrayexpress

p65

Project description:p65

| PRJNA811604 | ENA

Myeloid cell RelA/p65 promotes lung cancer proliferation

2012-04-01 | GSE36568 | GEO

Trancriptome profiling of murine overexpression of p65/RelA mutants

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in DA1-3B Bcr-Abl+ murine cell lines

2022-07-27 | GSE98437 | GEO

Transcriptome profiling of murine overexpression of p65/RelA mutants II

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in B16 Bcr-Abl+ murine cell lines

2022-07-27 | GSE135136 | GEO

Transcriptome profiling of murine overexpression of p65/RelA mutants III

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in DA1-3B Bcr-Abl+ murine cell lines

2022-07-27 | GSE135137 | GEO

Analysis of glucocorticoid receptor (NR3C1), NFkb (p65 subunit), and RNA polymerase 2 (RNAP2) binding in Beas-2B airway epithelial cells

Project description:The objective of this study was to determine binding patterns for GR, 65 and RNAP2 in Beas-2B airway epithelial cells after treatment with dexamethasone (100 nm), TNF (20 ng/ml) or both for one hour. This study utilized duplicate samples for each treatment condition and immunoprecipitation except for p65 immunoprcipitation of TNF treated samples, which was analyzed as a single sample. Input from vehicle treated cells was used a control. Experimental comparisons were made between the following samples/ treatment conditions. Duplicate samples of Beas-2B cells treated with ethanol (vehicle) were used for ChIP of GR, p65, and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with dexamethasone were used for ChIP of GR and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with TNF were used for ChIP of p65 and RNAP2 (1 sample p65, 2 samples RNAP2). Duplicate samples of Beas-2B cells treated with dexamethasone + TNF were used for ChIP of GR, p65 and RNAP2 (2 samples each antibody).

2016-04-01 | E-GEOD-79803 | biostudies-arrayexpress

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. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

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

Effect of S534A substitution in the p65 subunit of Nfkb on response to 1mg LPS

Project description:WT mice and Nfkb/p65 S534A were exposed to 1mg/kg LPS and their gene expression measured. Affymetrix Mouse 1.0ST chips were used to measure gene expression.

2017-04-05 | GSE67178 | GEO

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