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Effect of Eya3 knockdown and constitutively-active NF-kB add-back (IKK2-SE) in 66cl4 cells in vitro

ABSTRACT: Effect of Eya3 knockdown and constitutively-active NF-kB add-back (IKK2-SE) in 66cl4 cells in vitro

PROVIDER: PRJNA1216787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32162761_1.fastq.gz	Fastqsanger.gz
	SRR32162761_2.fastq.gz	Fastqsanger.gz
	SRR32162762_1.fastq.gz	Fastqsanger.gz
	SRR32162762_2.fastq.gz	Fastqsanger.gz
	SRR32162763_1.fastq.gz	Fastqsanger.gz

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Effect of Eya3 knockdown and constitutively-active NF-kB add-back (IKK2-SE) in 66cl4 cells in vitro

Project description:To investigate gene expression changes associated with Eya3 knockdown and add-back of constitutively-active NF-kB (IKK2-SE) in 66cl4 cells

2025-05-14 | GSE288294 | GEO

Transcription profiling by array of murine cardiomyocytes with and without expression of constitutively active IKK2

Project description:Inflammation is a major factor in heart disease. IÎºB kinase (IKK) and its downstream target NF-ÎºB are regulators of inflammation and are activated in cardiac disorders, but their precise contributions and targets are unclear. We analyzed IKK/NF-ÎºB function in the heart by a gain-of-function approach, generating an inducible transgenic mouse model with cardiomyocyte-specific expression of constitutively active IKK2 (IKK2-CA). In adult animals, IKK2 activation led to inflammatory dilated cardiomyopathy and heart failure. Transgenic hearts showed infiltration with CD11b+ cells, fibrosis, fetal reprogramming, and atrophy of myocytes with strong constitutively active IKK2 expression. To gain insight into proximal events after activation of IKK2/NF-ÎºB, we isolated cardiomyocytes and activated the transgene in vitro, thus avoiding interference of other cell types. Gene expression analysis revealed up-regulation of transcripts of chemotactic cytokines, adhesion molecules, and a striking number of IFN-regulated genes in cardiomyocytes expressing IKK2-CA. In addition, apoptotic and anti-apoptotic genes were up-regulated.

2015-10-19 | E-MTAB-3975 | biostudies-arrayexpress

Gene expression analysis of hematopoietic stem progenitor cells from transgenic mice that express the constitutively active form of IKK2 protein in HSCs

Project description:To understand molecular mechanisms that are deregulated in hematopoietic stem progenitor cells from transgenic mice that express the constitutively active form of IKK2 protein in HSCs (CA/CA mice), we isolated Flt3 low Lin-Sca1+c-Kit+ (LSK) cells from control and CA/CA mice and performed microarray analysis using the Illumina's MouseWG-6 v2.0 Expression BeadChip platform.

2018-10-13 | GSE121195 | GEO

Gene expression data from murine heart ventricles E12.5 with and without cardiomyocyte-specific expression of constitutively active IKK2

Project description:The transcription factor NF-κB has been associated with a range of pathological conditions of the heart, mainly based on its function as a master regulator of inflammation and pro-survival factor. Here, we addressed the question what effects activation of NF-κB can have during murine heart development. We expressed a constitutively active (CA) mutant of IKK2, the kinase activating canonical NF-κB signaling, specifically in cardiomyocytes under the control of the α-myosin heavy chain promoter. Expression of IKK2-CA resulted in embryonic lethality around E13. Embryos showed defects in compact zone formation and the contractile apparatus, and overall were characterized by widespread inflammation with infiltration of myeloid cells. Gene expression analysis at E12.5 suggested an interferon type I signature, with increased expression of interferon regulatory factors.

2015-10-14 | E-MTAB-3971 | biostudies-arrayexpress

Ikk2 regulates cytokinesis during vertebrate development (Trancriptome profiling from the wild-type and Ikk2 maternal-zygotic mutant zebrafish)

Project description:Purpose: The Ikk2 maternal-zygotic mutants are the only vertebrates animals completely depleted globally of the Ikk2 function which is expected to block an activity of the canonical NFkB signaling pathway. Transcriptome profiling of embryos before the midblastula transition (MBT) and after MBT may provide a clean strategy to identify the NFkB target genes. Methods: Zebrafish lines were maintained under standard laboratory procedures. Results: Using an optimized data analysis workflow, we identified 54,276 transcripts in the embryos at 2 hours postfertilization (hpf) and 4 hpf. RNA-seq data confirmed lack of expression of a number of genes in the mutant both prior to and after the MBT, including genes linked to angiogenesis, skin development, cytokinesis, innate immunity and cytoskeletonT, and 4 of these were validated with qRT–PCR. M. add here if required. Conclusions: Our study represents the first detailed analysis of transcriptomes of vertebrates globally depleted of activity of Ikk2, with two biologic replicates, generated by RNA-seq technology.The data reported here should provide a framework for understanding of maternal and zygotic genes which expression is controlled by Ikk2 activity. Our results expands a list of transcripts which expression may be controlled by the canonical NFkB signaling. We conclude that RNA-seq based transcriptome characterization improves analysis of NFkB regulated genes.

2017-08-21 | GSE90971 | GEO

Gene expresssion changes in pancreatic islets of 11 weeks old IKK2-CApdx-1 mice compared to control and Pdx-1+/- mice

2014-05-02 | GSE47504 | GEO

RNAseq of Trypanosoma brucei brucei EATRO1125 bloodstream forms without EIF4E2 compared with add-back

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Complementary and countervailing actions of Jak2 and Ikk2 in hematopoiesis in mice

Project description:Hyperactivation of JAK2 kinase is a unifying feature of human Ph- myeloproliferative neoplasms (MPNs), most commonly due to the JAK2 V617F mutation. Mice harboring a homologous mutation in the Jak2 locus exhibit a phenotype resembling polycythemia vera. NFκB pathway hyperactivation is present in myeloid neoplasms, including MPNs, despite scarcity of mutations in NFκB pathway genes. To determine the impact of NFκB pathway hyperactivation in conjunction with Jak2 V617F, we utilized Ikk2 (Ikk2-CA) mice. Pan-hematopoietic Ikk2-CA alone produced depletion of hematopoietic stem cells and B cells. When combined with the Jak2 V617F mutation, Ikk2-CA rescued the polycythemia vera phenotype of Jak2 V617F. Likewise, Jak2 V617F ameliorated defects in hematopoiesis produced by Ikk2-CA. Single-cell RNA sequencing of hematopoietic stem and progenitor cells revealed multiple genes antagonistically regulated by Jak2 and Ikk2, including subsets whose expression was altered by Jak2 V617F and/or Ikk2-CA but partly or fully rectified in the double mutant. We hypothesize that Jak2 promotes hematopoietic stem cell population self-renewal, whereas Ikk2 promotes myeloid lineage differentiation, and biases cell fates at several branch points in hematopoiesis. Jak2 and Ikk2 both regulate multiple genes affecting myeloid maturation and cell death. Therefore, the presence of dual Jak2 and NFκB hyperactivation may present neomorphic therapeutic vulnerabilities in myeloid neoplasms.

2025-04-07 | GSE263101 | GEO

Expression data comparing the effect of IKK2 KO on a KRAS mouse model

Project description:Given that the NF-κB pathway plays an important role in tumor development and that IKK2 is the seminal kinase responsible for NF-κB pathway activation, we were particularly interested in exploring the therapeutic potential of IKK2 inhibition in non-small cell lung cancers. We crossed IKK2fl/fl and KrasG12D mice so that we could simultaneously activate KrasG12D to initiate tumor formation and inactivate IKK2, upon transduction by Cre lentiviral vectors.

2011-12-15 | GSE30049 | GEO

Gene expresssion changes in pancreatic islets of 11 weeks old IKK2-CApdx-1 mice compared to control and Pdx-1+/- mice

Project description:Canonical IKK/NF-κB signaling is a master regulator of inflammation and innate immunity and has been implicated in the pathogenesis of T1D. To investigate the impact of NF-κB activation on β-cell homeostasis and diabetes development, we generated a transgenic gain-of-function mouse model allowing conditional NF-κB activation via expression of IKK2-CA (constitutively active IKK2 allele) in β-cells using the tetracycline-regulated gene expression system. Pdx-1-tTA (knockin model generating Pdx-1 haploinsufficiency) driver mice were used for β-cell specific transgene expression. Double transgenic IKK2-CA-pdx-1 mice develop a full-blown immune-mediated diabetes.To identify gene expression changes underlying this diabetes development pancreatic islets of diabetic IKK2-CA-Pdx-1, PDX-1 +/- and control mice were prepared and isolated total RNA was used for microarray analysis. Pancreatic islets were isolated from 11 weeks old control (n=5), Pdx-1+/- (n=4) and IKK2-CApdx-1 (n=5) mice, total RNA was extracted with RNeasy mini kit (QIAGEN). Microarray analyses were performed using 200 ng total RNA as starting material and 5.5 µg ssDNA per hybridization (GeneChip Fluidics Station 450; Affymetrix, Santa Clara, CA). The total RNAs were amplified and labeled following the Whole Transcript (WT) Sense Target Labeling Assay (http://www.affymetrix.com). Labeled ssDNA was hybridized to Mouse Gene 1.0 ST Affymetrix GeneChip arrays (Affymetrix, Santa Clara, CA). The chips were scanned with a Affymetrix GeneChip Scanner 3000 and subsequent images analyzed using Affymetrix® Expression Console Software (Affymetrix). Probe level data were obtained using the robust multichip average (RMA) normalization algorithm.

2014-05-02 | E-GEOD-47504 | biostudies-arrayexpress

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