Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of genes regulated by IKKb (Ird5) in the presence or absence of CrPV (Cricket paralysis virus) infection in Drosophila S2 cells

ABSTRACT: This DNA microarray analysis (agilent) helps to identify candidate genes regulated by IKKb (Ird5) on Non-infected condition and after CrPV infection (2h and 6h).

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE99044 | GEO | 2018/08/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Analysis of IKKb (Ird5) regulated genes in control and hemizygote IKKb (Ird5) null mutant adult flies after DCV (Drosophila C virus) infection

Project description:This DNA microarray analysis (agilent) help to identify candidate genes induced by DCV infection and regulated by IKKb (Ird5) in control (Df/+) and hemizygote IKKb (Ird5) null mutant (Dr/Ird5[1]) adult flies.

2018-08-14 | GSE99043 | GEO

Compensatory IKKa activation of classical NF-kB signaling during IKKb inhibition

Project description:A subtype of diffuse large B-cell lymphoma (DLBCL), termed activated B-cell-like (ABC) DLBCL, depends on constitutive NF-kB pathway signaling for survival. Small molecule inhibitors of IkB kinase b (IKKb), a key regulator of the NF-kB pathway, kill ABC DLBCL cells and hold promise for the treatment of this lymphoma type. We conducted an RNA interference genetic screen to investigate potential mechanisms of resistance of ABC DLBCL cells to IKKb inhibitors. We screened a library of small hairpin RNAs (shRNAs) targeting 500 protein kinases for shRNAs that would kill an ABC DLBCL cell line in the presence of a small molecule IKKb inhibitor more effectively than in its absence. Two independent shRNAs targeting IKKa synergized with the IKKb inhibitor to kill three different ABC DLBCL cell lines but were not toxic by themselves. Surprisingly, IKKa shRNAs blocked the classical rather than the alternative NF-kB pathway in ABC DLBCL cells, as judged by inhibition of IkBa phosphorylation. IKKa shRNA toxicity was reversed by coexpression of wild type but not kinase inactive forms of IKKa, suggesting that IKKa may directly phosphorylate IkBa under conditions of IKKb inhibition. These results suggest that therapy for ABC DLBCL may be improved by targeting both IKKa and IKKb. Keywords: compound treatment design Gene expression profiling of OCI-Ly3 cells with or without expressing IKKa shRNA in the presence or absence of 12.5 uM IKKb inhibitor for 2 and 3 days. Four samples were analyzed.

2009-06-01 | E-GEOD-11902 | biostudies-arrayexpress

Effect of tubular IKKb deletion in acute ischemic kidney injury

Project description:To establish the role of Ikkb during acute kidney injury, we use a mouse line with a specific deletion of Ikkb in the renal tubular system and exposed them to ischemia/reperfusion. Sample collection were done 2 days and 14 days after ischemia/reperfusion.

2022-07-09 | GSE207430 | GEO

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

Project description:To investigate NF-kB-driven gene expression in IEC, we performed microarray analysis from enterocytes of mice that express a constitutively active form of IKKb in intestinal epithelial cells Total RNA was prepared from enterocytes obtained from small intestines of IKKb(EE)IEC and WT littermates. Two biological replicates were performed for each experimental condition.

2011-06-09 | E-GEOD-29701 | biostudies-arrayexpress

Compensatory IKKa activation of classical NF-kB signaling during IKKb inhibition

2009-06-01 | GSE11902 | GEO

Transmission of Cricket paralysis virus via exosome-like vesicles during infection of Drosophila cells

Project description:Examining the role of exosomes in the life cycle of CrPV in Drosophila Melanogaster. sing prquantitative proteomics we find CrPV proteins in exosome-like vesicles, which upon further aanalysis appear to facilitate infection.

2018-11-14 | PXD011271 | Pride

BRCA1-mimetic compound NSC35446.HCl inhits IKKB expression by reducing estrogen receptor alpha occupancy in the IKKB promoter and inhibts NF-κB activity in anti-estrogen resitant human breast cells

Project description:We previously identified small molecules that fit into a BRCA1-binding pocket within estrogen receptor-alpha (ER), mimic the ability of BRCA1 to inhibit ER activity (“BRCA1-mimetics”), and overcome antiestrogen resistance. One such compound, the hydrochloride salt of NSC35446 (“NSC35446.HCl”), also inhibited growth of antiestrogen-resistant LCC9 tumor xenografts. The purpose of this study was to investigate the down-stream effects of NSC35446.HCl and its mechanism of action. Methods: Here, we studied antiestrogen-resistant (LCC9, T47DCO, MCF-7/RR, LY2), ER-negative (MDA-MB-231, HCC1806, MDA-MB-468), and antiestrogen-sensitive (MCF-7) cell lines. Techniques utilized include RNA-seq, qRT-PCR, cell growth analysis, cell-cycle analysis, Western blotting, luciferase reporter assays, TUNEL assays, in-silico analysis of the IKKB gene, and ChIP assays. Results: NSC35446.HCl inhibited proliferation and induced apoptosis in antiestrogen resistant LCC9, T47DCO, MCF-7/RR, and LY2 cells but not in ER-negative breast cancer cell lines. IKKB (IKKβ, IKBKB), an upstream activator of NF-B, was identified as a BRCA1-mimetic-regulated gene, based on an RNA-seq analysis; and NSC35446.HCl inhibited IKKB mRNA and protein expression in LCC9 cells. NSC35446.HCl also inhibited NF-B activity and expression of NF-B target genes. In-silico analysis of the IKKB promoter identified nine estrogen response element (ERE) half-sites and one ERE-like full-site. ChIP assays revealed that ER was recruited to the ERE-like full-site and five of the nine half-sites and that ER recruitment was inhibited by NSC35446.HCl in LCC9 and T47DCO cells. Conclusions: These studies identify functional EREs in the IKKB promoter and identify IKKB as an NSC35446.HCl-regulated gene; and they suggest that NF-B and IKKB, which were previously linked to antiestrogen resistance, are targets for NSC35446.HCl in reversing antiestrogen resistance.

2017-07-21 | GSE101691 | GEO

Transcriptome analysis of annotated coding genes and sORF in 16 organs and 17 environmental conditions at A. thaliana

Project description:There are 16 organ samples (dry seeds, 24H imbibed seeds, 48H imbibed seeds, juvenile rosette, adult rosette, senescence leaves, cauline leaves, stems, young buds, mature flower buds, flowers, young siliques, mature siliques and old siliques) with triplicates. There are 17 samples of different environmental samples (0 h white, 1 h white, 6 h white, 24 h white, dark, blue, far-red and red lights, control, cold 2h, cold 6h, hot 2h, hot 6h, NaCl 2h, NaCl 6h, dry 2h and dry 6h) with triplicates.

2012-09-30 | GSE34188 | GEO

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

2011-06-09 | GSE29701 | GEO

Transcriptional responses of mantle cell lymphoma (MCL) lines to IKKB inhibition

Project description:MCL cell lines were treated with DMSO or 5uM AFN700 for 20hrs This experiment is designed to see if NFKB-target genes are downregulated by inhibition of IKKB in MCL cell lines that are insensitive to ibrutinib (BTK inhibitor) or sotrastaurin (PKC inhibitor) MCL cells were seeded in 6well dishes and treated for 20hrs with DMSO or 5uM AFN700

2013-12-01 | E-GEOD-52434 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data