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RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375 (replicate 2).

ABSTRACT: RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375 (replicate 2).

PROVIDER: PRJNA416128 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6230590_1.fastq.gz	Fastqsanger.gz
	SRR6230590_2.fastq.gz	Fastqsanger.gz
	SRR6230591_1.fastq.gz	Fastqsanger.gz
	SRR6230591_2.fastq.gz	Fastqsanger.gz
	SRR6230592_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375 (replicate 2).

Project description:Introduction: there is growing evidence that the IFN-γ-related cytokine signature plays a major role supporting the effect of pharmacological blockade of immune checkpoints. The expression of IFN-γ in cancer cells is repressed by several factors, among them a key role is played by the oncogene EZH2, which in turns is controlled by the non-canonical NF-kB pathway and its upstream kinase, NIK. Methodology: we developed a series of NIK inhibitors and compared the effects on cancer cells of one of them (DMBP5) to an siRNA against NIK via transcriptomic analysis (RNA-seq). Results: mRNA modifications induced by DMBP5 on A375 melanoma cells closely resemble the ones observed with siRNA against NIK. Conclusions: DMBP5 is a very selective and effective non-competitive NIK inhibitor (first in class).

2020-01-08 | GSE106285 | GEO

RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375 (replicate 1)

2020-01-08 | GSE101637 | GEO

RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375

Project description:Introduction: there is growing evidence that the IFN- -related cytokine signature plays a major role supporting the effect of pharmacological blockade of immune checkpoints. The expression of IFN- in cancer cells is repressed by several factors, among them a key role is played by the oncogene EZH2, which in turns is controlled by the non-canonical NF-kB pathway and its upstream kinase, NIK. Methodology: we developed a series of NIK inhibitors and compared the effects on cancer cells of one of them (DMBP5) to an siRNA against NIK via transcriptomic analysis (RNA-seq). Results: mRNA modifications induced by DMBP5 on A375 melanoma cells closely resemble the ones observed with siRNA against NIK. Conclusions: DMBP5 is a very selective and effective non-competitive NIK inhibitor (first in class).

2020-01-08 | GSE106286 | GEO

RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375

Project description:RNA-Seq analysis of the impact of a kinase NIK inhibitor (DMBP5) on the human melanoma cell line A375

| PRJNA416122 | ENA

Constitutive activation of the receptor-like kinase NIK impairs translation and confers tolerance to begomovirus infection

Project description:To generate an efficient defense against begomovirus, we modulated the activity of the immune defense receptor NIK (NSP-Interacting Kinase) in tomato plants; NIK is a virulence target of the begomovirus NSP during infection. Replacing threonine-474 with aspartate (T474D) within the kinase activation loop promoted the constitutive activation of NIK-mediated defenses. This activation resulted in the down-regulation of translation-related genes and the suppression of global translation in T474D-overexpressing tomato lines. We also found that T474D-induced defense-related transcripts were associated with polysomes and immune proteins, which accumulated to detectable levels in T474D leaves. Consistent with these findings, T474D transgenic lines were tolerant to the tomato-infecting begomoviruses ToYSV and ToSRV. We propose that NIK mediates an anti-viral response via translation suppression and immune system induction. Global variation on gene expression induced by NIK expression and virus infection using total RNA from mock-inoculated and ToYSV-infected tomato wild-type plants, mock-inoculated and infected 35S::NIK1-4 overexpressing lines and mock-inoculated and infected 35S::T474D overexpressing lines. File map_itag23.csv correlates the ITAG 2.3 cDNA ID with the 21 bp reads in file Profiles_with_differential_expressions.csv.

2013-12-17 | E-GEOD-38028 | biostudies-arrayexpress

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

Constitutive activation of the receptor-like kinase NIK impairs translation and confers tolerance to begomovirus infection

2013-12-17 | GSE38028 | GEO

NF-κB-Inducing Kinase (NIK) Governs the Mitochondrial Respiratory Capacity, Differentiation, and Inflammatory Status of Innate Immune Cells

Project description:NF-κB-Inducing Kinase (NIK), which is essential for the activation of the noncanonical NF-κB pathway, regulates diverse processes in immunity, development, and disease. While recent studies have elucidated important functions of NIK in adaptive immune cells and cancer cell metabolism, the role of NIK in metabolic-driven inflammatory responses in innate immune cells remains unclear. Here we demonstrate that NIK-deficient bone marrow-derived macrophages exhibit defects in mitochondrial-dependent metabolism and oxidative phosphorylation (OXPHOS) functions that impair acquisition of a pro-repair, anti-inflammatory phenotype. Subsequently, NIK-deficient mice exhibit skewing of myeloid cells characterized by aberrant eosinophil, monocyte, and macrophage cell populations in the blood, bone marrow, and adipose tissue. Furthermore, NIK-deficient blood monocytes display hyperresponsiveness to bacterial lipopolysaccharide and elevated TNFα production ex vivo, indicative of systemic inflammation. These findings suggest that NIK is required for the metabolic rewiring of mitochondrial respiration that is critical for balancing pro- and anti-inflammatory myeloid immune cell functions. Overall, our work highlights a previously unrecognized role for NIK as a molecular rheostat that fine-tunes immunometabolism in innate immunity and suggests that metabolic dysfunction may be an important driver of inflammatory diseases caused by aberrant NIK expression or activity.

2023-01-20 | GSE223040 | 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

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

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