Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of gene expression in colorectal cancer cells with DGKG overexpression

ABSTRACT: To clarify the role of diacylglycerol kinase gamma (DGKG) in colorectal cancer, we carried out a gene expression microarray analysis using HCT116 cells infected with adenoviral vectors which express LacZ, kinase-dead mutant of DGKG (DGKG-KD) or constitutively active form of DGKG (DGKG-CA).

ORGANISM(S): Homo sapiens

PROVIDER: GSE92573 | GEO | 2017/03/01

SECONDARY ACCESSION(S): PRJNA358066

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of TTF-1/NKX2-1 expression on TGF-beta induced gene expression in A549 lung cancer cell line.

Project description:TTF-1/NKX2-1 was expressed by adenoviral vector and changes in gene expression were determined by RNA-sequencing. A549 cells were infected with Ad-TTF-1 or Ad-LacZ vectors and stimulated with TGF-beta for 24 hours or left untreated. Expression of polyA RNA was determined.

2014-07-27 | E-GEOD-56356 | biostudies-arrayexpress

Assessing the role of TPL2 in TauP301S mice

Project description:ScRNAseq analysis shows •TPL2 KD (kinase dead) reduced TauP301S dependent IEG and MHCII activation states in microglia •TPL2 KD reduced peripheral immune cell infiltration in TauP301S mouse brain

2022-07-16 | GSE180041 | GEO

RNA-sequencing of 7 weeks old mouse testes

Project description:We performed RNA-sequencing of testes derived from Atr+/+ or Atr+/KD 7 weeks old mice. Since Atr+/KD male mice are sterile and present severe spermatogenesis defects, we aimed at analyzing the possible changes in gene expression given by the ATR kinase-dead (KD) mutation

2018-12-17 | GSE122139 | GEO

Adenoviral vector vaccination induces a conserved program of CD8+ T cell memory differentiation in mouse and man

Project description:Following exposure to vaccines, antigen-specific CD8+ T-cell responses develop as long-term memory pools. Novel vaccine strategies based on adenoviral vectors, e.g. those developed for HCV, are able to induce and sustain substantial CD8+ T-cell populations. How such populations evolve following vaccination remains to be defined at a transcriptional level. We addressed the transcriptional regulation of divergent CD8+ T-cell memory pools induced by an adenoviral vector encoding a model antigen (beta-galactosidase). We observe transcriptional profiles that mimic those following infection with persistent pathogens, murine and human cytomegalovirus (CMV). Key transcriptional hallmarks include up-regulation of homing receptors, and anti-apoptotic pathways, driven by conserved networks of transcription factors, including T-bet (TBX21). In humans, a novel adenovirus vaccine induced similar CMV-like phenotypes and underlying transcription factor regulation. These data clarify the core features of CD8+ T-cell memory following vaccination with adenovirus vectors and indicate a conserved pathway for memory development shared with persistent herpesviruses. Total RNA was extracted from sorted memory CD8 T cells induce by CMV and adenoviral vectors, and naïve CD8 cells

2015-09-23 | E-GEOD-73314 | biostudies-arrayexpress

Transcription profiling of mouse fibroblast cells infected with adenoviral vector or mock infected

Project description:The innate immune response to 1st generation adenoviral vectors was ascertained through high level infection of primary cells from a inbred mouse strain, replete with an intact and functioning TLR system. Experiment Overall Design: Quiescent murine C57/Bl6 fibroblasts were Ad (E1-E3-LacZ at MOI=300) or Mock infected. Sixteen hrs post-infection, RNA was harvested, transcribe to cDNA and bitotin-labeled, and hybridized to Mu11k A and B arrays.

2007-12-04 | E-GEOD-3172 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow macrophages from WT and IRAK4 kinase

Project description:IRAK-4 is an essential component of the signal transduction complex downstream of the IL-1- and Toll-like receptors. Though regarded as the first kinase in the signaling cascade, the role of IRAK-4 kinase activity versus its scaffold function is still controversial. In order to investigate the role of IRAK-4 kinase function in vivo, âknock-inâ mice were generated by replacing the wild type IRAK-4 gene with a mutant gene encoding kinase deficient IRAK-4 protein (IRAK-4 KD). Analysis of bone marrow macrophages obtained from WT and IRAK-4 KD mice with a number of experimental techniques demonstrated that the IRAK-4 KD cells greatly lack responsiveness to stimulation with the Toll-like receptor 4 (TLR4) agonist LPS. One of the techniques used, microarray analysis, identified IRAK-4 kinase-dependent LPS response genes and revealed that the induction of LPS-responsive mRNAs was largely ablated in IRAK-4 KD cells. In summary, our results suggest that IRAK-4 kinase activity plays a critical role in TLR4-mediated induction of inflammatory responses. Experiment Overall Design: The response of mouse bone marrow macrophages from WT and IRAK4 kinase dead animals to stimulation with LPS at two time points was determined. There were 12 samples in total, 6 from WT and 6 from IRAK4 kinase dead cells; for each strain there were 3 conditions: growth for 4 hours without stimulation (the strain-specific control), growth for 1 hour with stimulation, and growth for 4 hours with stimulation; for each condition there were two biological replicates.

2008-10-20 | E-GEOD-9037 | biostudies-arrayexpress

Molecular basis of Tousled-Like-Kinase 2 (TLK2) activation – LC-MS/MS-based analysis of TLK2 phosphorylation state

Project description:In this study on human Tousled-Like-Kinase 2 (TLK2) mass spectrometry-based analysis was applied as part of a molecular characterization of TLK2 in the aim to increase the understanding of the mode of activation of this protein. Specifically, different TLK2 constructs were analyzed to generate a “phosphorylation map” of the TLK2 protein. To analyse the phosphorylation state of TLK2 we used recombinant protein purified from Escherichia coli. Samples of different TLK2 constructs were used for in-gel digestion and analysed by mass spectrometry. All samples were prepared and run in triplicates for label-free quantification. Explanation for MS raw files with TLK2 construct included: Ac: TLK2 construct consisting of amino acid residues 191-772 (Ac indicates active form). KD: TLK2 construct consisting of amino acid residues 191-772 with mutation D613A (KD indicates kinase-dead form). FusionKD: Kinase-dead part of a heterodimeric TLK2 construct (amino acid residues 191-772) with mutation D613A (KD indicates kinase-dead form). FusionAC: Active part of a heterodimeric TLK2 construct (amino acid residues 191-772) (Ac indicates kinase-dead form). KDlong: Kinase domain of TLK2 with C-tail (amino acid residues 450-772). KDshort: Kinase domain of TLK2 without C-tail (amino acid residues 450-753).

2018-10-23 | PXD007675 | Pride

A central helical hairpin in SPD-5 enables centrosome strength and assembly

Project description:Cross-linked samples consist of middle region of SPD-5 (541-677) plus 18 amino acids at the N-terminus (MGSSHHHHHHENLYFQSN) which we term F1. Two F1 samples (7.6 uM) were incubated with either kinase dead or constitutively active PLK-1 plus ATP-MgCl2 in a 150 mM KCl, 25mM HEPES, pH7.4 buffer for 2 hours at room temperature. Samples were then cross-linked using 8mM DMTMM for 45min and quenched with 50 mM ammonium bicarbonate for 15 min at RT shaking at 300rpm. Samples ran on a 16-20% SDS-page gel revealing a monomer band and a dimer band in both conditions using a coomassie based stain. Monomer bands (LUM2_1076612, PLK-1 KD, LUM2_1076614, PLK-1 -CA) and dimer bands (LUM2_1076613, PLK-1 KD, LUM2_1076615, PLK-1 KD) were excised.

2024-02-28 | MSV000094191 | MassIVE

Transcription profiling of mouse embryonic fibroblasts from wild type and IRAK-4 kinase dead animals stimulated with IL-1b for different durations to identify IRAK-4 kinase-dependent IL-1b response genes.

Project description:IRAK-4 is an essential component of the signal transduction complex downstream of the IL-1- and Toll-like receptors. Though regarded as the first kinase in the signaling cascade, the role of IRAK-4 kinase activity versus its scaffold function is still controversial. In order to investigate the role of IRAK-4 kinase function in vivo, knock-in mice were generated by replacing the wild type IRAK-4 gene with a mutant gene encoding kinase deficient IRAK-4 protein (IRAK-4 KD). Analysis of embryonic fibroblasts and macrophages obtained from IRAK-4 KD mice with a number of experimental techniques demonstrated that they greatly lack responsiveness to stimulation with IL-1b or a Toll-like receptor 7 (TLR7) agonist. One of the techniques used, microarray analysis, identified IRAK-4 kinase-dependent IL-1b response genes in mouse embryonic fibroblasts and revealed that the induction of IL-1b-responsive mRNAs was largely ablated in IRAK-4 KD cells. In summary, our results suggest that IRAK-4 kinase activity plays a critical role in IL-1R/TLR7-mediated induction of inflammatory responses. Experiment Overall Design: The response of mouse embryonic fibroblasts from WT and IRAK4 kinase dead animals to stimulation with IL-1b at two time points was determined. There were 12 samples in total, 6 from WT and 6 from IRAK4 kinase dead cells; for each strain there were 3 conditions: growth for 4 hours without stimulation (the strain-specific control), growth for 1 hour with stimulation, and growth for 4 hours with stimulation; for each condition there were two biological replicates.

2007-11-15 | E-GEOD-6789 | biostudies-arrayexpress

Adenoviral vector vaccination induces a conserved program of CD8+ T cell memory differentiation in mouse and man

2015-09-23 | GSE73314 | GEO