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The IL32/BAFF axis supports prosurvival dialog in the lymphoma ecosystem and is disrupted by NIK inhibition

ABSTRACT: The IL32/BAFF axis supports prosurvival dialog in the lymphoma ecosystem and is disrupted by NIK inhibition

PROVIDER: PRJNA744431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15058775.fastq.gz	Fastqsanger.gz
	SRR15058776.fastq.gz	Fastqsanger.gz
	SRR15058777.fastq.gz	Fastqsanger.gz
	SRR15058778.fastq.gz	Fastqsanger.gz
	SRR15058779.fastq.gz	Fastqsanger.gz

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Similar Datasets

The IL32/BAFF axis supports prosurvival dialog in the lymphoma ecosystem and is disrupted by NIK inhibition

Project description:We demonstrated that the microenvironment-dependent secretion of IL32β was controlled by the CD40L/NFKB2 axis whereas its tumor specificity was the consequence of IL32 promoter hypomethylation in MCL. Through the secretion of IL32β, the tumor was able to corrupt its microenvironment through the polarization of monocytes into specific MCL-associated macrophages, which in turn favor tumor survival. We next highlighted that while IL32β-stimulated macrophages secreted several protumoral factors, they supported tumor survival through a soluble dialog, mostly driven by BAFF. Finally, we demonstrated the efficacy of selective NIK/alternative-NFkB inhibition to counteract both microenvironment-dependent induction of IL32β and BAFF-dependent survival of MCL cells.

2022-12-06 | GSE179766 | GEO

The IL32/BAFF axis supports prosurvival dialog in the lymphoma ecosystem and is disrupted by NIK inhibition

2022-12-06 | GSE179636 | GEO

The IL32/BAFF axis supports prosurvival dialog in the lymphoma ecosystem and is disrupted by NIK inhibition

Project description:The IL32/BAFF axis supports prosurvival dialog in the lymphoma ecosystem and is disrupted by NIK inhibition

| PRJNA744918 | ENA

Investigating the effect of NIK SMI1, a small molecule inhibitor of NIK, on TWEAK-stimulated Mouse renal proximal tubule-interstitial epithelial cells (RPTEC)

Project description:Systemic lupus erythematosus (SLE) is often considered a disease driven by autoreactive B cells and anti-nuclear antibodies. However, therapeutic targeting of B cells, for example through BAFF blockade, has been only partially effective in SLE. NF-κB Inducing Kinase (NIK) mediates non-canonical NF-κB signaling downstream of disease relevant TNF family members, such as BAFF, TWEAK, CD40, and OX40. We hypothesized that NIK inhibition might be more efficacious than BAFF blockade in lupus, and therefore generated highly selective and potent small molecule inhibitors (SMI) of NIK to test this hypothesis. RNASeq was used to investigate the effects of one of these SMIs of NIK, NIK SMI1, on TWEAK-stimulated Mouse renal proximal tubule-interstitial epithelial cells (RPTEC).

2017-10-26 | GSE89195 | GEO

NIK expression stimulated G6PD phosphorylation

Project description:Our findings establish NIK as a pivotal regulator of T cell metabolism in anti-tumor immunity and highlight a posttranslational mechanism of metabolic regulation involving the G6PD-NADPH redox system. CoIP assays revealed a strong physical interaction between NIK and G6PD in both T cells and transiently transfected 293 cells, suggesting G6PD to be a direct target of NIK. Using a phosphoprotein gel analysis approach, we demonstrated that NIK expression stimulated G6PD phosphorylation. To further study the mechanism, we performed mass spectrometry identify phosphorylation sites of G6PD stimulated by NIK

2020-10-05 | PXD020943 | Pride

Delta4-BAFF an new transcription factor

Project description:The purpose of the study was to identify downstream gene targets regulated by a new alternative splice of BAFF (B-Cell Activating factor belonging to the TNF Family) that we called Delta4-BAFF (because it characterized by an alternative splice of exon 4). To do this we used human burkitt's lymphoma cell line (RAMOS) stably transfected with Delta4-BAFF or stably transfected with Delta4-BAFF mutated on its N-glycosylation site (Delta4-BAFF-N124D). One control was used : RAMOS stably transfected with empty vector (pIRES2-GFP from Clontech)

2012-09-28 | E-MEXP-3595 | biostudies-arrayexpress

Comparasion between MCF7-NIK overexpressing cells, MCF7-control cells and MCF7-NIK depleted cells

Project description:Analysis of differentially expressed genes in MCF7 cancer cells transfected with an expression vector containing the ORF of NIK, a shRNA of NIK and a control shRNA. Transient transfections were performed in triplicates . We use micorarrays to elucidate the machanisms by which NIK regulates stem cells biology

2015-11-30 | GSE63382 | GEO

RNA-seq Analysis of Transcriptomes in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing αTC1-6 cells

Project description:Purpose: The goal of this study is to determine the molecular mechanisms involved in the NIK regulation of α cell function. Methods: mRNA profiles of β-Gal control, NIK, and NIK(KA) overexpressed αTC1-6 cells were generated by deep sequencing using an Illumina Hiseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.89) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of NIK-overexpressing aTC1-6 cell transcriptomes, generated by RNA-seq technology. Our results show that 328 genes were upregulated and 48 genes were downregulated following NIK overexpression. GO analysis indicated that the upregulated genes were primarily related to the immune response. KEGG pathway enrichment analysis showed that immune signaling pathways, including the TNF, NF-κB, and chemokine signaling pathways, were significantly activated by NIK overexpression in aTC1-6 cells, while genes related to metabolism-associated signal pathways were significantly decreased. NIK(KA), the dominant-negative mutant of NIK, does not affect gene expression in aTC1-6 cells.

2018-12-30 | GSE112511 | GEO

BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

Project description:Emerging clinical evidence points to a function for B cell activating factor (BAFF) in pregnancy. However, a direct role for BAFF-axis members including BAFF, the closely related a proliferation-inducing ligand (APRIL), and their respective receptors in pregnancy has not been examined. This study demonstrates that loss of BAFF results in decreased inflammatory responsiveness and decreased susceptibility to inflammation-induced preterm birth (PTB). In contrast, loss of APRIL increases inflammatory responsiveness and susceptibility to PTB. Consistent with overlapping receptor utilization by BAFF and APRIL, deletion of BAFF-axis receptors is not sufficient to modify susceptibility to PTB. Critically, therapeutic administration of BAFF/APRIL monoclonal antibodies or recombinant proteins is sufficient to manipulate susceptibility to inflammation-induced PTB. Further, macrophages are identified as the principle BAFF producing immune cells at the maternal-fetal interface and BAFF and APRIL divergently manipulate macrophage gene expression and inflammatory function. Genes linked to labor initiation are upregulated in WT and APRIL deficient macrophages while downregulated in BAFF deficient macrophages and correlate with myeloid gene expression in human placental samples during labor. Thus, BAFF and APRIL play important, but divergent, counterregulatory inflammatory roles in pregnancy and provide new therapeutic targets for mitigating the risk of PTB.

2023-08-03 | GSE202811 | GEO

NIK/NF-kappaB2 regulated gene products.

Project description:This study aims at identifying genes that are NIK/NF-kappaB2 responsive in murine dendritic cells matured in vivo. Keywords: NIK/NF-kappaB2 responsive genes in dendritic cells after TLR/CD40 signaling

2008-03-05 | GSE7219 | GEO

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