Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151093 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Dendritic cells (DC) play central roles in coordinating appropriate immune responses to pathogens. In the present study, the genes regulated by NFkB activators, RelB and cRel, in PAMP-induced bone marrow dendritic cells (BMDCs) activation was examined. Total RNA extracted from WT, relb-/-, crel-/-relb-/- bone marrow derived dendritic cells (BMDCs) were subjected to stimulation with CpG or Pam3CSK4.
2012-10-01 | E-GEOD-34990 | biostudies-arrayexpress
Project description:NF-kappaB Activation Model includes the activation of both NFKB1:RELA and NFKB2:RELB for Canonical and Non-Canonical Pathway respectively.
The model includes the pathway model integrated with post-translational modifications of NF-kB subunits that regulate the NFKB1:RELA and NFKB2:RELB activity. The processes that are regulated by NF-kB pathway can be monitored through following readouts NFKB1:RELA Activity, NFKB2:RELB Activity, Degraded RelA, Degraded RelB, Degraded IkB, Degraded NIK, Apoptosis, Tumour, Antiviral Activity, B Cell Growth and Cell Migration. However, last 5 processes above are also influenced by other pathways too, therefore while making predictions, caution has to be exercised.
2022-05-27 | MODEL2001290001 | BioModels
Project description:Dendritic cells (DC) play central roles in coordinating appropriate immune responses to pathogens. In the present study, the genes regulated by NFkB activators, RelB and cRel, in PAMP-induced bone marrow dendritic cells (BMDCs) activation was examined.
2012-10-01 | GSE34990 | GEO
Project description:Malignant Hodgkin's lymphoma (HL) cells are characterized by constitutive activation of the canonical as well as the non-canonical NF-κB signaling cascades. We depleted subunit combinations corresponding to either canonical (p50/RelA) or non-canonical (p52/RelB) dimers in the HL cell line L-1236 and performed Affymetrix microarray analysis. Knockdown of p52/RelB affected the expression of a significantly higher number of genes than the knockdown of p50/RelA. The two sets of target genes presented a partial overlap, however they also revealed specific genes that are involved in distinct aspects of tumor biology. The knockdown of subunit combinations corresponding to either canonical (p50/RelA, experimental group 1) or non-canonical (p52/RelB, experimental group 2) NF-κB heterodimers were carried out in L-1236 cells. Two distinct siRNA sequences for every NF-κB subunit and two non-targeting siRNA sequences (control) were used for each experimental group. Experiments were performed in biological triplicates.
2016-02-18 | E-GEOD-64232 | biostudies-arrayexpress
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:Pro-inflammatory cytokines were shown to promote growth and survival of cancerous cells. TNF induced RelA:p50 NF-κB dimer via the canonical pathway is thought to link inflammation with cancer. Integrating biochemical and computational studies we identify that deficiency of non-canonical signal transducer p100 triggers a positive autoregulatory loop, which instead perpetuates an alternate RelB:p50 containing NF-κB activity upon TNF treatment. TNF stimulated RelB:p50 dimer is sufficient for mediating NF-κB target gene-expressions and suppressing apoptotic cellular death independent of principal NF-κB subunit RelA. We further demonstrate that activating mutations in non-canonical NF-κB module deplete multiple myeloma cells of p100, thereby, provoking autoregulatory RelB:p50 activation. Finally, autoregulatory control reinforces protracted pro-survival NF-κB response, albeit comprising of RelB:p50, upon TNF priming that protects myeloma cells with dysfunctional p100 from subsequent apoptotic insults. In sum, we present evidence for positive autoregulation mediated through the NF-κB system and its potential involvement in human neoplasm.
2017-06-12 | GSE68615 | GEO
Project description:Mesenchymal stem cells (MSCs) are known to induce the conversion of activated T-cells into regulatory T-cells in vitro. The marker CD69 is a target of canonical NF-κB signaling and is transiently expressed upon activation; however, stable CD69 expression defines cells with immunoregulatory properties. Given its enormous therapeutic potential, we explored the molecular mechanisms underlying the induction of regulatory cells by MSCs. Peripheral blood CD3+ T-cells were activated and cultured in the presence or absence of MSCs. CD4+ cell mRNA expression was then characterized by microarray analysis. The drug BAY11-7082 and a siRNA against RELB were used to explore the differential roles of canonical and non-canonical NF-κB signaling, respectively. Flow cytometry and real-time PCR were used for analyses. Genes with immunoregulatory functions, CD69 and non-canonical NF-κB subunits (RELB and NFKB2) were all expressed at higher levels in lymphocytes co-cultured with MSCs. The frequency of CD69+ cells among lymphocytes cultured alone progressively decreased after activation. In contrast, the frequency of CD69+ cells increased significantly following activation in lymphocytes co-cultured with MSCs. Inhibition of canonical NF-κB signaling by BAY immediately following activation blocked the induction of CD69; however, inhibition of canonical NF-κB signaling on the 3rd day further induced the expression of CD69. Furthermore, late expression of CD69 was inhibited by RELB siRNA. These results indicate that the canonical NF-κB pathway controls the early expression of CD69 after activation; however, in an immunoregulatory context, late and sustained CD69 expression is promoted by the non-canonical pathway and is inhibited by canonical NF-κB signaling. In order to study the molecular basis by which Multipotent Mesenchymal Stromal/Stem Cells (MSC) exert their immune regulatory function, immunomagnetically purified CD3+ T-cells from the peripheral blood of 3 individuals were activated and cultured in the presence or absence of MSCs. Following 5 days, CD4+ and CD8+ T-cells were further immunomagnetically selected and their gene expression profiles were obtained by microarrays and compared. Paired samples from 3 individuals were used for this analysis.
2011-08-02 | E-GEOD-31153 | biostudies-arrayexpress
Project description:Malignant Hodgkin's lymphoma (HL) cells are characterized by constitutive activation of the canonical as well as the non-canonical NF-κB signaling cascades. We depleted subunit combinations corresponding to either canonical (p50/RelA) or non-canonical (p52/RelB) dimers in the HL cell line L-1236 and performed Affymetrix microarray analysis. Knockdown of p52/RelB affected the expression of a significantly higher number of genes than the knockdown of p50/RelA. The two sets of target genes presented a partial overlap, however they also revealed specific genes that are involved in distinct aspects of tumor biology.
2016-02-18 | GSE64232 | GEO
Project description:Dysfunction of the non-canonical NF-kB signaling pathway has been causally associated with numbers of cancers and autoimmune diseases. However, specific inhibitors for this signaling pathway remain to be developed. Here we showed that structure-based cell-based screening yielded a potent and specific small molecule targeting RelB to inhibit non-canonical NF-kB signaling pathway, while had no inhibitory effect on canonical NF-kB signaling pathway. Mechanistically, the inhibitor directly interacted with RelB protein and disrupted RelB binding to its target DNA, thus repressing RelB transactivity on target genes. Through blocking oncogenic activity of non-canonical NF-kB signaling pathway in colorectal cancer or B lymphoma, the inhibitor efficiently exerted a potent antitumor effect in vitro and in vivo. Thus, our study provided new RelB-targeting inhibitor that inhibited non-canonical NF-kB signaling pathway and facilitated precise therapeutic applications in cancers and possibly other diseases.
2025-04-23 | GSE288086 | GEO
Project description:The malignant cells of Hodgkin's lymphoma are characterized by a constitutive activation of the canonical as well as the non-canonical NF-κB signaling cascades. We carried out genome-wide localization and expression profiling experiments in the Hodgkin lymphoma cell line L1236 for the canonical and non-canonical NF-κB pathway components p65, p50 and p52, RelB, respectively. We found that the single NF-κB subunits bind to overlapping, but distinct cistromes by using consensus motifs of high similarity. ChIP-Seq analysis of 4 NF-κB subunits with 2 biological replicates each
2016-02-18 | E-GEOD-63736 | biostudies-arrayexpress