Genome-wide differential binding pattern of NFKB2/p52 under prolonged culture conditions
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ABSTRACT:
PROVIDER: PRJNA755535 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15499629.fastq.gz | Fastqsanger.gz | |||
| SRR15499630.fastq.gz | Fastqsanger.gz | |||
| SRR15499631.fastq.gz | Fastqsanger.gz |
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Project description:We report the application of ChIP-Seq analysis for high-throughput profiling of NFKB2/p52 binding pattern under prolonged culture conditions. Briefly, we investigate the genome wide binding behavior of endogenous p52 in WI-38 cells. The cells was cultured with regular DMEM medium for prolonged time (7 days). Chromatin immunoprecipitated DNA was converted to libraries for sequencing with HiSeq 4000. We find that there is a distinct binding pattern of p52 under prolonged culture condtion. This study provides a preliminary but solid basis to our understanding of NFKB2/p52 binding dynamics during aging process.
2022-04-13 | GSE182248 | GEO
Project description:The alternative (non-canonical) nuclear factor-kappa B (NF-κB) signalling pathway predominantly regulates the function of the p52/RelB heterodimer. Germline Nfkb2 deficiency in mice leads to loss of p100/p52 protein and offers protection against a variety of gastrointestinal conditions, such as azoxymethane/dextran sulfate sodium (DSS)-induced colitis-associated cancer and lipopolysaccharide (LPS)-induced small intestinal epithelial apoptosis. However, the common underlying protective mechanisms are not yet fully understood. Here we applied RNA sequencing and identified a B-lymphocyte defect as the major signature in the small intestinal mucosa of naïve adult Nfkb2-/- mice. Proteomics analysis also revealed a dramatic decrease in small intestinal immunoglobulin A levels, and this was validated by quantitative ELISA in both small intestinal lysates and serum. Moreover, the numbers of IgA-producing, CD138+ve plasma cells were also reduced in the lamina propria of the small intestinal villi of Nfkb2-/- mice. This phenotype was even more striking in the small intestinal mucosa of RelB-/- mice, although these mice were equally sensitive to LPS-induced intestinal apoptosis as their RelB+/+ wild-type counterparts. Therefore, p52 deficiency offers resistance to LPS-induced intestinal apoptosis and appears to regulate the plasma cell population within the gut.
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Project description:Dendritic cells (DCs) orchestrate intestinal inflammation in health and diseases. We found that human IBD was associated with heightened non-canonical NF-κB signaling in intestinal DCs. The non-canonical NF-κB pathway, which induces RelB:p52-mediated immune gene expressions, has been implicated in DC functions and that genetic inactivation of RelB:p52 in DCs alleviated experimental colitis in mice. Here, we aim to investigate the regulation of gene expression by noncanonical Nfkb2 pathway in modulating DC function.
2024-06-11 | GSE249101 | GEO
Project description:To investigate the effects of NFKB signaling, RNA-seq analysis was performed on both Jurkat and MT-2 cells. It was observed that either NFKB1 or NFKB2 knockout could alter the gene expression profile in MT-2 cells compared to Jurkat cells. Gene expression profiles of NFKB1/NFKB2 knockout Jurkat cells were compared to the mock edited Jurkat cells. On the other hand, it was hypothesized that the gene expression profile of MT-2 cells can be more drastically altered by NFKB1 or NFKB2 knockout. NFKB2 knockout MT-2 cells exhibited a unique gene expression profile compared to those of NFKB1 knockout MT-2 cells and mock edited MT-2 cells.
2023-11-01 | E-MTAB-13408 | biostudies-arrayexpress
Project description:To understand the mechanism by which p52 expression augments tumorigenesis, gene expression microarray analysis was performed using mRNA isolated from lungs of CCSP-p52 and WT mice on dox for 1 week to identify genes with altered expression in CCSP-p52 mice. The microarray dataset includes eight samples, with two replicates for each combination of two factors (p52 and LPS).Since samples with and without LPS stimulation were processed and microarray profiled at the same time, we assumed the random data variations were similar across all samples and built a linear model across the eight samples accounting for both p52 and LPS experimental factors. The coefficient (estimated log fold change) and p-value associated with the p52 factor were retrieved for the selection of differentially expressed genes. When selecting top-ranking p52-induced genes, only probe sets mapping to known genes and having positive expression changes were considered. While the used microarrays were Affymetrix Mouse Gene 1.0 ST arrays, in the later step of probe set annotation we used annotation table associated with Mouse Gene 1.1 ST (GPL11533 table). The Robust Multichip Average method implemented in R package “oligo” (v1.28.3) was employed to normalize imported raw data. Probe sets interrogating control, unmapped, or intron sequences were ignored, leaving 79% of probe sets for a differential expression analysis. Linear models and empirical Bayes methods implemented in R package “limma” (v3.20.8) were applied to estimate log fold changes and p-values for the p52-vs-WT effect.
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Project description:This study systematically analyzed the molecular mechanism and function of nuclear factor kappa B subunit 2 (NFKB2) in colorectal cancer (CRC) to investigate the potential of NFKB2 as a therapeutic target for CRCTo investigate the potential of NFKB2 as a therapeutic target for colorectal cancer (CRC), we conducted a systematic analysis of the molecular mechanism and function of NFKB2 in CRC. VariousA range of experimental techniques, including RNA sequencing, proteome chip assays, and small molecule analysis, were used to obtaingain a deeper understanding of the regulation of NFKB2 in CRC. TheOur results revealed that NFKB2 was upregulated in a significant proportion of patients with advanced hepatic metastasismetastases of CRC. NFKB2 played an importanta role in promoting tumor growth through CD8+ T cell exhaustion. MoreoverAdditionally, NFKB2 directly interacted with signal transducer and activator of transcription 2 (STAT2)STAT2, leading to increased phosphorylation of STAT2 and the upregulation of programmed death ligand 1 (PD-L1)PD-L1 expression. Applying aThe application of a small molecule inhibitor of NFKB2 (Rg5) led to a reduction in PD-L1 expression and improved response to programmed death-1 (PD-1)PD-1 blockade-based immunotherapy. In conclusion,These findings suggest that the facilitated NFKB2-STAT2/PD-L1 axis may suppresses immune surveillance in CRC and targeting NFKB2 maycould enhance the efficacy of immunotherapeutic strategies. Our resultsThis study provides novel insights into the molecular mechanisms underlying the contribution of NFKB2 in CRC immune escape. However, our findings requireand further validation of these findings in a clinical trial is needed to establish NFKB2 inhibition as a therapeutic strategy for CRC patients.
2023-12-21 | GSE250065 | GEO
Project description:Role of NFKB2 in pancreatic ductal adenocarcinama (PDAC)
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Project description:Homologous recombination (HR) serves multiple roles in DNA repair that are essential for maintaining genomic stability. The central HR protein, RAD51, is frequently overexpressed in human malignancies, thereby elevating HR proficiency and promoting resistance to DNA-damaging therapies. Here we find that non-canonical NF-κB factors control the expression of RAD51 andother HR-promoting proteins. Transcriptional silencing of p100/p52 reduces RAD51 protein levels in multiple human cancer subtypes. RNA-seq after p100/p52 silencing identifies RAD51 as the most differentially expressed gene among 40 genes with known relevance to HR. While p100/p52 depletion inhibits HR function in human tumor cells, it does not influence the function of other double-strand DNA repair pathways including single-strand annealing, microhomology mediated annealing, or non-homologous end joining.
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Project description:As such, TNF triggers the canonical NF-?B pathway to induce a nuclear NF-?B activity composed of the RelA:p50 dimer in WT cells. Nfkb2 encodes p100, which regulates the activity of the RelB NF-?B heterodimers during immune cell-differentiation via the noncanonical pathway. Our biochemical analyses revealed that an absence of p100 instead repositions RelB under the control of the TNF-activated canonical pathway. Indeed, chronic TNF treatment of Nfkb2-/- cells activates the RelA:p50 dimer and an additional RelB:p50 dimer. On the other hand, TNF stimulation of Relb-/-Nfkb2-/- and Rela-/-Nfkb2-/- MEFs exclusively activated the RelA:p50 dimer and the RelB:p50 dimer, respectively. We treated this panel of knockout MEFs with TNF for 6h before being subjected to microarray mRNA analysis. We also included in our analysis WT MEFs and Rela-/-Relb-/-Rel-/- MEFs, which served as a negative control. Our analyses revealed overlapping and distinct gene-expression specificities of RelA:p50 and RelB:p50 dimers activated in mutant cells in response to TNF.
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