Similar studies for GEO DataSets (Select 200053835) - GEO DataSets

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Items: 20

Select item 2000538351.

Pathological activation of canonical nuclear-factor kB by synergy of tumor necrosis factor alpha and TNF-like weak inducer of apoptosis in mouse acute colitis

(Submitter supplied) To test the efficacy of TNFR-Fc and anti-TWEAK mAb treatment alone and in combination Tumor necrosis factor (TNF)-alpha is a major effector in various inflammatory conditions. TNF-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily that promotes inflammatory tissue damage through its receptor, FGF-inducible molecule 14 (Fn14). Since both TWEAK and TNF-alpha have been shown to mediate pathological responses through inter-dependent or independent pathways by in vitro, the potential interplay of these pathways was investigated in a mouse colitis model. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
72 Samples

Download data: CEL

Series

Accession:: GSE53835

ID:: 200053835

Select item 2000250292.

Ionizing radiation in GI tract of Tweak KO mice

(Submitter supplied) TWEAK/Fn14 signaling may regulate the expression of genes involved in epithelial repair and mucosal inflammation. Comparing the gene signatures in WT and TWEAK KO mice will inform the biology of TWEAK/Fn14 pathway in the GI tract.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
56 Samples

Download data: CEL, TXT

Series

Accession:: GSE25029

ID:: 200025029

Select item 2002730633.

Profile of gene expression in experimental acute kidney injury

(Submitter supplied) Treatment for acute kidney injury (AKI) is suboptimal. A better understanding of its pathogenesis may lead to new therapeutic approaches. Kidney transcriptomics analyses of murine folic acid-induced AKI (FA-AKI) will allow us to identify new mediators and therapeutic targets of this pathology. Folic acid nephropathy is a classical model of AKI characterized by acute renal failure, tubular cell death, interstitial leukocyte infiltration and subsequent tubular regeneration that has been reported in humans.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL6246
6 Samples

Download data: CEL, XLS

Series

Accession:: GSE273063

ID:: 200273063

Select item 2000368064.

Chronic TNBS Colitis in the FN14 KO Mouse

(Submitter supplied) To test TWEAK/Fn14 pathway and relative agents in chronic TNBS colitis

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
23 Samples

Download data: CEL

Series

Accession:: GSE36806

ID:: 200036806

Select item 2001199615.

Immune differentiation regulator p100 tunes NF-kB responses to TNF

(Submitter supplied) Stringent regulation of TNF signaling prevents aberrant inflammation. TNF engages the canonical NF-kB pathway for activating the RelA:p50 heterodimer, which mediates specific expressions of pro-inflammatory and immune response genes. Importantly, the NF-kB system discriminates between time-varied TNF inputs. Negative feedback regulators of the canonical pathway, including IkBa, thought to ensure transient RelA:p50 responses to brief TNF stimulations. more...

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL19057
9 Samples

Download data: TXT

Series

Accession:: GSE119961

ID:: 200119961

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001485776.

An epithelial Nfkb2 pathway exacerbates intestinal inflammation by supplementing latent RelA complexes to the canonical NF-kB module

(Submitter supplied) The canonical NF-kB module induces nuclear translocation of RelA heterodimers from the latent cytoplasmic complexes. RelA directs inflammatory immune responses against microbial entities. However, aberrant RelA activity also triggers destructive inflammation, including those associated with inflammatory bowel disease (IBD). What provokes this pathological RelA activity remains unclear. As such, the noncanonical NF-kB pathway activates RelB heterodimers and mediates immune organogenesis. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
12 Samples

Download data: TXT

Series

Accession:: GSE148577

ID:: 200148577

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000686157.

An autoregulatory RelB:p50 NF-κB pathway perpetuates pro-survival TNF response in multiple myeloma

(Submitter supplied) Pro-inflammatory cytokines were shown to promote growth and survival of cancerous cells. TNF induced RelA:p50 NF-κB dimer via the canonical pathway is thought to link inflammation with cancer. Integrating biochemical and computational studies we identify that deficiency of non-canonical signal transducer p100 triggers a positive autoregulatory loop, which instead perpetuates an alternate RelB:p50 containing NF-κB activity upon TNF treatment. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL6885
12 Samples

Download data: TXT

Series

Accession:: GSE68615

ID:: 200068615

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000848588.

The Molecular Mechanism for EZH2 Function in DSS-induced Colitis

(Submitter supplied) Here we employed the genetically engineered mice models (GEM) to uncover the role of gut epithelial EZH2 in the pathogenesis of colitis. To dissect the underlying mechanism, Chip-Seq analysis is used for mechanistic study. From the result we find EZH2 mainly targeted in the TSS region. As we have known TNF-alpha pathway can be regulated by EZH2, we try and find TRAF2/5 may be the key point for EZH2 to regulated TNF-alpha pathway. more...

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL19057
2 Samples

Download data: BW

Series

Accession:: GSE84858

ID:: 200084858

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000848579.

The Role of Epithelium EZH2 in Experimental Colitis

(Submitter supplied) Despite recent progress, the contribution of epigenetic mechanisms to govern Inflammatory bowel disease (IBD) pathogenesis remains elusive. Here we show that epithelial EZH2, the catalytic subunit of PRC2 is critical for experimental colitis. Depletion of EZH2 in intestinal epithelial cells sensitized the cells to DSS-induced colitis in mice. To dissect underlying mechanism, we conducted gene expression profile analysis (RNA-Seq) by using primary Intestinal epithelial cells (IECs) isolated from EZH2 WT and KO mice to gain molecular insights into the affected biological processes. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
4 Samples

Download data: TXT

Series

Accession:: GSE84857

ID:: 200084857

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20027306410.

Profile of gene expression in murine tubular cells MCTs treated with the cytokine TWEAK

(Submitter supplied) Treatment of acute kidney injury (AKI) is suboptimal. TWEAK is known to mediate cell death and inflammation in AKI. Transcriptomic analysis of murine tubular cells will allow us to identify novel mediators and therapeutic targets of this pathology. TWEAK is an inflammatory cytokine which is upregulated in AKI. Transcriptomic analysis of TWEAK-stimulated cultured murine tubular epithelial cells identified downregulation of peroxisome proliferator activated receptor-g coactivador-1a (PGC-1a) and its target genes (mitochondrial proteins Ndufs1, Sdha, and Tfam) as a shared feature.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL6246
6 Samples

Download data: CEL, XLS

Series

Accession:: GSE273064

ID:: 200273064

Select item 20000894211.

Mouse colon expression in wild type and STAT5b deficient mice

(Submitter supplied) Regulation of epithelial barrier function is dependent upon precise control of cell survival and activation of inflammatory pathways in response to the enteric flora. These experiments tested differential colon gene expression relative to these pathways in wild type and STAT5b deficient mice. Keywords: Single time point in wild type and STAT5b deficient mice.

Organism:: Mus musculus

Type:: Expression profiling by array

Dataset:: GDS3385
Platform:: GPL5759
8 Samples

Download data: CEL

Series

Accession:: GSE8942

ID:: 200008942

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 338512.

Transcription factor STAT5b deficiency effect on the colon

Analysis of colons of animals lacking the Signal Transducers and Activators of Transcription member STAT5b. STAT5b mutants are more susceptible to experimental colitis, associated with intestinal barrier function defects. Results provide insight into the role of STAT5b in colonic barrier function.

Organism:: Mus musculus

Type:: Expression profiling by array, transformed count, 2 genotype/variation sets

Platform:: GPL5759
Series:: GSE8942
8 Samples

Download data: CEL

DataSet

Accession:: GDS3385

ID:: 3385

PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet

Select item 20000887113.

Human Breast Cancer Cell Lines: Control vs. Fn14 or Luciferase siRNA Treated

(Submitter supplied) We performed gene expression profiling on the MDA-MB-231 and MDA-MB-436 human breast cancer cell lines following siRNA-mediated inhibition of Fn14 expression as an approach to identify the mechanistic basis for Fn14 regulation of invasive capacity. Keywords: siRNA-mediated inhibition

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL887
8 Samples

Download data: TXT

Series

Accession:: GSE8871

ID:: 200008871

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20015317814.

Mouse colon organoids treated with inflammatory reagents.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by array

Platforms:: GPL21810 GPL10787
15 Samples

Download data: TXT

Series

Accession:: GSE153178

ID:: 200153178

Select item 20015317615.

Gene expression of mouse colon organoids treated with inflammatory reagents.

(Submitter supplied) Microarray analysis of mouse colon organoids after treatment with the mixture of inflammatory reagents.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL10787
9 Samples

Download data: TXT

Series

Accession:: GSE153176

ID:: 200153176

Select item 20015317516.

Gene expression of mouse colon organoids after the removal of inflammatory reagents.

(Submitter supplied) Microarray analysis of mouse colon organoids after the removal of inflammatory reagents following long-term treatment with inflammatory reagents.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL21810
6 Samples

Download data: TXT

Series

Accession:: GSE153175

ID:: 200153175

Select item 20000096917.

Anti-GBM antibody effect on kidney

(Submitter supplied) Control total RNA, pooled from the kidney of five normal BALB/c mice, was used as a reference against total RNA extracted from the kidney of BALB/c mice injected with anti-GBM antibody for 1, 3, 7, 11 and 16 days. This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by array

Dataset:: GDS580
Platform:: GPL254
15 Samples

Download data

Series

Accession:: GSE969

ID:: 200000969

Select item 58018.

Glomerulonephropathy

Gene expression profiling of anti-glomerular basement membrane (GBM) glomerulonephropathy model. Analysis of kidney tissue of BALB/c mice injected with anti-GBM antibody for 1, 3, 7, 11 or 16 days.

Organism:: Mus musculus

Type:: Expression profiling by array, log ratio, 5 time sets

Platform:: GPL254
Series:: GSE969
15 Samples

Download data

DataSet

Accession:: GDS580

ID:: 580

Select item 20023784519.

The TNFSF12/TWEAK modulates colonic inflammatory fibroblast differentiation and promotes fibroblast-monocyte interactions

(Submitter supplied) Fibroblasts acquire a pro-inflammatory phenotype in inflammatory bowel disease (IBD), but the factors driving this process and how fibroblasts contribute to the immune response is incompletely understood. The TNF superfamily factor 12 (TWEAK) has gained interest as a mediator of chronic inflammation. Here, we explore its role as a driver of inflammatory responses in fibroblasts and its contribution to fibroblast-monocyte interaction using human primary colonic fibroblasts, THP1 and peripheral blood mononuclear cells (PBMC). more...