Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [TLR]

ABSTRACT: Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [TLR]

PROVIDER: PRJNA449900 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains

Project description:Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains

| PRJNA449868 | ENA

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [NFkB]

Project description:Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [NFkB]

| PRJNA449901 | ENA

Benchmarking NF-kB inhibitors

Project description:Benchmarking NF-kB inhibitors

| PRJNA562687 | ENA

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [TLR]

Project description:comparing different lineages of M.tb strains (lineages 3 and 4) in interrupting of epithelial signalling pathways in A549 cell line, from TLRs and NFkB signalling pathways to specific cytokine secretion

2018-04-13 | GSE112998 | GEO

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-04-13 | GSE113051 | GEO

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [NFkB]

2018-04-13 | GSE113050 | GEO

The NF-kB genomic landscape in lymphoblastoid B-cells

Project description:The nuclear factor kB (NF-kB) subunits RelA, RelB, c-Rel, p50 and p52 are each critical for B-cell development and function. To systematically characterize their responses to canonical and non-canonical NF-kB pathways activity, we performed ChIP-seq analysis in lymphoblastoid B-cells. We found a surprisingly complex NF-kB binding landscape, which did not readily reflect the two NF-kB pathway paradigm. Instead, ten subunit binding patterns were observed at promoters and eleven at enhancers. Surprisingly, nearly one-third of NF-kB binding sites lacked kB motifs. De novo motif finding uncovered distinct modes of NF-kB recruitment at these sites. The oncogenic forkhead box protein FOXM1 and NF-kB co-occupied many kB sites despite the absence of a FOXM1 DNA motif. FoxM1 knockdown decreased expression of key NF-kB targets and caused apoptosis. Our study highlights opportunities for selective therapeutic NF-kB blockade. ChIP-seq was used to define the genomic landscape of NF-kB DNA binding in lymphoblastoid cells.

2014-08-29 | E-GEOD-55105 | biostudies-arrayexpress

Role of NF-kB in aging

Project description:To address the role of NF-kB in aging in vivo, we utilized a well-characterized system that allows inducible and site-specific inhibition of NF-kB activity in murine skin. The hormone binding domain of the mutant estrogen receptor that is responsive to 4-hydroxytamoxifen (4-OHT) was fused to a mutant of p50 (IDNkB, inducible dominant negative NF-kB) that dimerizes with other NF-kB subunits but is unable to bind DNA, thus dominantly inhibiting NF-kB activity. Expression was driven within the basal layer of murine epidermis by the keratin 14 promoter in transgenic mice. To test whether NF-kB activity is required to maintain age-associated gene expression, we applied topical 4-OHT and ethanol vehicle (EtOH) for two weeks to the right (R) and left (L) dorsal flanks, respectively, of chronologically aged transgenic mice (O, 18-23 months). Young transgenic mice (Y, 1 month) were treated in parallel as control. Skin samples were harvested and analyzed for gene expression using mouse cDNA microarrays containing 35,217 elements, representing 18,880 unique genes. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set Computed

2010-06-30 | E-GEOD-3845 | biostudies-arrayexpress

The NF-kB genomic landscape in lymphoblastoid B-cells

2014-08-29 | GSE55105 | GEO

The IKK2/NF-kB-pathway suppresses MYC-induced lymphomagenesis

Project description:Abstract. Deregulated c-MYC is found in a variety of cancers where it promotes proliferation as well as apoptosis. In many hematological malignancies enhanced NF-kB exerts prosurvival functions. Here we investigated the role of NF-kB in mouse and human c-MYC-transformed lymphomas. The NF-kB-pathway is extinguished in murine lymphoma cells and extrinsic stimuli typically inducing NF-kB activity fail to activate this pathway. Genetic activation of the NF-kB pathway induces apoptosis in these cells, while inhibition of NF-kB by an IkBa superrepressor provides a selective advantage in vivo. Furthermore, in human Burkitt´s lymphoma cells we find that NF-kB activation induces apoptosis. NF-kB upregulates Fas and predisposes to Fas-induced cell death, which is caspase 8 mediated and can be prevented by CFLAR overexpression. We conclude that c-MYC overexpression sensitizes cells to NF-kB-induced apoptosis and persistent inacvtivity of NF-kB signaling is a prerequisite for MYC-mediated tumorigenesis. We could also show that low immunogenicity and Fas insensitivity of MYC driven lymphoma cells is reversed by activation of NF-kB. Our observations provide a molecular explanation for the described absence of the NF-kB signaling in Burkitt´s lymphoma and question the applicability of NF-kB inhibitors as candidates for treatment of this cancer.

2009-07-22 | GSE17129 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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