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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE63382 | GEO | 2015/11/30

SECONDARY ACCESSION(S): PRJNA267604

REPOSITORIES: GEO

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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

Transcriptional responses of mantle cell lymphoma (MCL) after NIK knockdown

Project description:MCL lines were treated with or without 100ng/ml doxycycline for 7 days This experiment is designed to see if shRNA-mediated knockdown of NIK downregulates NFKB signaling in MCL lines with mutations in upstream regulators of the alternative pathway (TRAF2 & TRAF3) MCL cells carrying inducible non-targeting control (NTC) shRNA, NIKshRNA#1 (NIKsh#1), or NIKshRNA#2 (NIKsh#2) were seeded in 6well dishes and treated for 7 days with or without 100ng/ml doxycycline.

2013-12-01 | E-GEOD-52435 | biostudies-arrayexpress

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

Transcriptional responses of mantle cell lymphoma (MCL) after NIK knockdown

2013-12-01 | GSE52435 | GEO

RNA-seq analysis of mRNA profiles in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing INS-1 832/13 cells

Project description:Purpose: The goal of this study is to investigate how NIK regulates islet β-cell function. Methods: mRNA profiles of β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing INS-1 832/13 cells were generated by deep sequencing using an Illumina Hiseq platform. Paired-end clean reads were aligned to the rat reference genome (ftp://ftp.ensembl.org/pub/release-90/fasta/rattus_norvegicus/dna/) 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 mRNA profiles in NIK-overexpressing and NIK(KA)-overexpressing INS-1 832/13 cells, generated by RNA-seq technology. Our results show that 471 genes were upregulated and 249 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, antigen processing and presentation signaling pathways, were significantly activated by NIK overexpression in INS-1 832/13 cells, whereas genes related to insulin secretion and regulation of secretion were significantly decreased. NIK(KA), the dominant-negative mutant of NIK, does not induce the expression of genes related to immune response in INS-1 832/13 cells.

2020-07-28 | GSE130121 | GEO

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/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

Global variation of gene expression induced by constitutive activation of the NIK receptor in Arabidopsis

Project description:Arabidopsis was transformed with the NIK receptor or the mutant T474D NIK receptor and infected with CaLCuV. The global variation of gene expression was analysed by RNA-seq at 10 days post inoculation and 20 days post inoculation and differential gene expression was determinated in comparison with mock inoculated Arabidopsis lines. Pairwise comparison between mock inoculated and infected genotypes (WT,NIK-expressing lines and T474D-expressing lines) at 10 dpi and 20 dpi

2014-04-21 | E-GEOD-56922 | biostudies-arrayexpress

Expression data from MCF7 cells: control or tuberin-depleted

Project description:Analysis of the expression profiles of MCF7 cells transduced with a control shRNA and an TSC2-targeted shRNA (leading to tuberin depletion).

2015-04-28 | GSE68324 | GEO

The NFKB inducing kinase (NIK) modulates hematopoiesis during stress

Project description:The genetic programs that maintain hematopoiesis during steady state in physiologic conditions are different from those activated during stress. Here we show that hematopoietic stem cells (HSCs) with deficiencies in components of the alternative NFkB pathway (the NFkB inducing kinase, NIK, and the downstream molecule NFkB2) had a defect in response to stressors such as supraphysiological doses of cytokines, chemotherapy and hematopoietic transplantation. NIK-deficient mice had peripheral blood and bone marrow leukocyte numbers within normal ranges (except for the already reported defects in B-cell maturation), however, HSCs showed significantly slower expansion capacity in in vitro cultures compared to wild type HSCs. This was due to a delayed cell cycle and increased apoptosis. In vivo experiments showed that NIK-deficient HSCs did not recover at the same pace as controls when challenged with myeloablative chemotherapy. Finally, NIK-deficient HSCs showed a significantly decreased competitive repopulation capacity in vivo. Using HSCs from mice deficient in one of two downstream targets of NIK, i.e., either NFkB2 or c-Rel, only NFkB2 deficiency recapitulated the defects detected with NIK-deficient HSCs. Our results underscore the role of NIK and the alternative NFkB pathway for the recovery of normal levels of hematopoiesis after stress.

2014-11-29 | GSE63702 | GEO

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