Nfkb2 deficiency and its impact on the murine small intestinal mucosa
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB47948 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6912740_1.fastq.gz | Fastqsanger.gz | |||
| ERR6912740_2.fastq.gz | Fastqsanger.gz | |||
| ERR6912741_1.fastq.gz | Fastqsanger.gz | |||
| ERR6912741_2.fastq.gz | Fastqsanger.gz | |||
| ERR6912742_1.fastq.gz | Fastqsanger.gz |
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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.
2022-07-31 | E-MTAB-11018 | biostudies-arrayexpress
Project description:Porcine small intestinal mucosa Raw sequence reads
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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: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:In this study, we applied the isobaric tags for relative and absolute quantitation (iTRAQ) technique to detect alterations in the proteomic profile of the jejunal mucosa using a porcine model in which piglets were offered the protein-limited (PL) diet. Protein identification and quantification for iTRAQ experiments were performed using ProteinPilot (v4.0.8085) software. The LC-MS/MS data were searched against the UniProtKB (sus scrofa). To minimize the false discovery rate (FDR), a threshold for protein identification was applied, with the confident value > 95% (amount to the confident value “unused ProtScore” > 1.3 in ProteinPilot software), and at least one unique peptide was considered for protein identification. Proteins that were quantified with fold change > 2.0 were considered to be differentially expressed proteins. We identified 5275 proteins, 202 of which were differentially expressed. Furthermore, we adopted function annotation analysis of all identified proteins and function enrichment analysis of all differentially expressed proteins to explore more meaningful proteins and pathways.
2016-12-22 | PXD004069 | Pride
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.
2019-06-13 | GSE99980 | GEO
Project description:The goal of the present study was to determine whether loss of the insulin receptor alters the molecular landscape of the intestinal mucosa, using intestinal-epithelial insulin receptor knockout (IE-irKO) mice and both genetic (IRfl/fl and Villin-cre) controls. Quantitative proteomic analysis by Liquid Chromatography Mass Spectrometry (LC-MS) was deployed on jejunal and colonic mucosa from mice fed a chow- or Western diet (WD). Jejunal mucosa from IE-irKO mice demonstrated alterations in all intestinal cell linages, Paneth, goblet, absorptive and enteroendocrine cells, whereas only goblet and absorptive cells were affected in the colon. There was also a significant effect of the WD on the gut proteome. A significant reduction was detected in Paneth cell proteins with anti-microbial activity, including lysozyme C-1, angiogenin-4, cryptdin-related sequence1C-3 and -2, a-defensin 17 and intelectin-1a. The key protein expressed by goblet cells, mucin-2, was also reduced in the IE-irKO mice. Proteins involved in lipid metabolism, including aldose reductase-related protein 1, 15-hydroxyprostaglandin dehydrogenase [NAD(+)], apolipoprotein A-II and pyruvate dehydrogenase kinase isozyme 4, were increased in the mucosa of WD-fed IE-irKO mice as compared to controls. In contrast, expression of the nutrient-responsive gut hormones, glucose-dependent insulinotropic polypeptide and neurotensin, was reduced in the jejunal mucosa of IE-irKO mice, and there was a reduction in proteins of the P-type ATPases and the solute carrier-transporter family in the colon of WD-fed IE-irKO mice. In conclusion, IE-irKO mice display a distinct molecular phenotype, suggesting a biological role of insulin and its receptor in determining differentiated cell-specificity in the intestinal epithelium.
2017-08-18 | PXD005932 | Pride
Project description:pig intestinal mucosa-associated microbiota Metagenome
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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