Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA270498 | ENA |
REPOSITORIES: ENA
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Project description:Malignant cells of Hodgkin's lymphoma (HL) cells are characterized by constitutive activation of the canonical as well as the non-canonical NF-κB signaling cascades. Knockdown of a subunit combination corresponding to the non-canonical NF-κB dimer (p52/RelB) in the HL cell line L-1236 caused up-regulation of a set of genes that are associated with hematopoietic and lymphoid organ development. As p52 can form homodimeric complexes, which can repress transcription either alone or in association with transcriptional repressors such as HDAC1, we knocked down p52 alone to analyze its role in gene repression in HL cells. We found that the single knockdown of p52 is indeed sufficient to up-regulate an interesting set of genes that may play a role in B-cell and/or HL development.
2016-12-21 | GSE64234 | GEO
Project description:Gene expression profiles of canonical and non-canonical NF-κB signaling pathways in Hodgkin’s lymphoma
| PRJNA270499 | ENA
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.
2016-02-18 | GSE63736 | 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.
2016-02-18 | GSE64232 | GEO
Project description:RNA-seq was used to characterize the NF-κB transcription factor -mediated regulation of B-cell genome wide target genes upon inducible LMP1 expression . We created an inducible stable EBV-negative Akata Burkitt Lymphoma cell line expressing LMP1 wildtype followed by stable CRISPR knockout of the individual NF-κB transciption factors (p52, RelB, p50, cRel or RelA) and 24 hours 250ng/ml doxycycline-induced LMP1 expression.
2024-01-30 | GSE247495 | 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:By binding to specific DNA elements, known collectively as “κB sites”, contained within the promoters/enhancers of target genes, NF-κB regulates gene expression. We found that the identity of the central base pair (bp) of κB sites profoundly impacts the transcriptional activity of NF-κB dimers. RelA dimers prefer an A/T bp at this position for optimum transcriptional activation (A/T-centric) and discriminate against G/C-centric κB sites. The p52 homodimer, in contrast, activates transcription from G/C-centric κB sites in complex with Bcl3 but represses transcription from the A/T-centric sites. The p52:Bcl3 complex binds to these two classes of κB sites in distinct modes permitting recruitment of coactivator, corepressor, or both coactivator and corepressor complexes in promoters containing G/C, A/T or both G/C and A/T-centric sites. Therefore, through sensing of bp differences within κB sites, NF-κB dimers modulate biological programs by activating, repressing and altering expression of effector genes. Total RNA extracted from bone marrow derived macrophages (BMDMs) with Bcl3 siRNA knockdown or mouse scramble siRNA knockdown were subjected to LPS stimulation.
2012-08-06 | E-GEOD-39922 | 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:In multiple myeloma, abnormal plasma cells establish oncogenic niches within the bone marrow by engaging the NF-κB pathway to nurture their survival while they accumulate pro-proliferative mutations. Under these conditions, many cases eventually develop genetic abnormalities endowing them with constitutive NF-κB activation. Here, we find that sustained NF-κB/p52 levels resulting from such mutations favours the recruitment of enhancers beyond the normal B-cell repertoire. Furthermore, through targeted disruption of p52, we characterise how such enhancers are complicit in the formation of super-enhancers and the establishment of cis-regulatory interactions with myeloma dependencies during constitutive activation of p52. Finally, we functionally validate the pathological impact of these cis-regulatory modules on cell and tumour phenotypes using in vitro and in vivo models, confirming RGS1 as a novel p52-dependent myeloma driver. We conclude that the divergent epigenomic reprogramming enforced by aberrant non-canonical NF-κB signalling potentiates transcriptional programs beneficial for multiple myeloma progression.
2024-03-01 | GSE230466 | GEO
Project description:In multiple myeloma, abnormal plasma cells establish oncogenic niches within the bone marrow by engaging the NF-κB pathway to nurture their survival while they accumulate pro-proliferative mutations. Under these conditions, many cases eventually develop genetic abnormalities endowing them with constitutive NF-κB activation. Here, we find that sustained NF-κB/p52 levels resulting from such mutations favours the recruitment of enhancers beyond the normal B-cell repertoire. Furthermore, through targeted disruption of p52, we characterise how such enhancers are complicit in the formation of super-enhancers and the establishment of cis-regulatory interactions with myeloma dependencies during constitutive activation of p52. Finally, we functionally validate the pathological impact of these cis-regulatory modules on cell and tumour phenotypes using in vitro and in vivo models, confirming RGS1 as a novel p52-dependent myeloma driver. We conclude that the divergent epigenomic reprogramming enforced by aberrant non-canonical NF-κB signalling potentiates transcriptional programs beneficial for multiple myeloma progression.
2024-03-01 | GSE230296 | GEO