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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

Mouse kidney after systemic endotoxin challenge

(Submitter supplied) 8 week-old male C57BL6J mice were given Gram-negative endotoxin (LPS O111:B4, 10 mg/kg) intraperitoneally at time 0. 18 hrs thereafter, they were administered 10 ml/kg 0.9% saline. Mice were sacrificed at 0, 18, or 42 hrs after LPS challenge. Kidneys were immediately collected into TRIzol for RNA preparation. Renal function was measured on blood collected at the time of tissue harvest At t=0hr, mice had normal baseline renal function. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL8760 GPL8759
24 Samples
Download data: CEL, CHP
Series
Accession:
GSE30576
ID:
200030576
5.

Loss of renal tubular PGC-1α exacerbates diet-induced renal steatosis and age-related urinary sodium excretion in mice

(Submitter supplied) The kidney has a high energy demand and is dependent on oxidative metabolism for ATP production. Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is highly expressed in kidney, its role in renal physiology is so far unclear. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
16 Samples
Download data: CEL
Series
Accession:
GSE80618
ID:
200080618
6.

Effects of Peroxisome proliferator-γ coactivator-1α (PGC-1a) isoform over-expression +/- TNFalpha on hepatocyte gene expression

(Submitter supplied) PGC-1a is a transcriptional coactivator known to regulate a broad gene program of nutrient and mitochondrial metabolism. Many splice variants of this protein have been identified, but their functions were unknown. This experiment was designed to delineate the downstream targets of two different PGC-1alpha isoforms (PGC-1a1 and PGC-1a4) in hepatocytes, and to determine whether inflammatory signaling (via TNFR activation) modulated these targets Liver is exposed to constantly changing metabolic and inflammatory environments. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
18 Samples
Download data: CEL, CHP
Series
Accession:
GSE132458
ID:
200132458
7.

Gene expression profiling of Huh-7 cells tranfected NC or DEPDC1 siRNA

(Submitter supplied) Many reports shows that DEPDC1 is up-regulated in many tumor types and promotes cell proliferation and invasion, thereby functioning as an oncogene. Hepatocellular Carcinoma has been shown to overexpress DEPDC1, and up-regulated DEPDC1 associates with poorer prognosis.In addition, we found that DEPDC1 knockdown significantly inhibited HCC cell proliferation, colony formation and migration. In order to investigate the mechanism of DEPDC1 in regulating HCC progression, we performed gene array analysis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
2 Samples
Download data: CEL, CHP
Series
Accession:
GSE122124
ID:
200122124
8.

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
9.

Genome-wide analysis of PGC-1α-binding in microglia

(Submitter supplied) PGC-1α in microglia protects against ischemia-induced brain damage in mice. The data suggest that microglia-specific PGC-1α play a key role in limiting ischemia-induced brain damage and potently participates in regulating microglial function. To further clarify the mechanism of PGC-1α, we conducted chromatin immunoprecipitation-sequencing (ChIP-Seq) analysis to identify the targets of PGC-1α in microglia from mPGC-1α mice at 24 h after ischemic stroke. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
4 Samples
Download data: WIG
Series
Accession:
GSE165564
ID:
200165564
10.

Gene expression profiles in microglia with or without PGC-1α overexpression after acute ischemic stroke (AIS)

(Submitter supplied) PGC-1α overexpression in microglia protects against ischemia-induced brain damage in mice. To investigate the underlying mechanism of PGC-1α, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes with the potential to change the microglial function. Indeed, PGC-1α overexpression alters the gene expression profiles of microglia after AIS, this suggested that microglial PGC-1α might play an important role after ischemic stroke.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL21163
6 Samples
Download data: TXT
Series
Accession:
GSE152871
ID:
200152871
11.

Gene expression profiles in BV2 cells with or without PGC-1α overexpression after LPS stimulation

(Submitter supplied) PGC-1α overexpression in microglia protects against ischemia-induced brain damage in mice. To investigate the underlying mechanism of PGC-1α in vitro, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes with the potential to change the BV2 cells function. Indeed, PGC-1α overexpression alters the gene expression profiles of BV2 cells, this revealed that PGC-1α could inhibit the production of IL-1β and pro-inflammatory cytokines.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL21163
6 Samples
Download data: TXT
Series
Accession:
GSE152769
ID:
200152769
12.

Gene expression profiles in microglia with or without PGC-1α overexpression

(Submitter supplied) PGC-1α overexpression in microglia protects against ischemia-induced brain damage in mice. To investigate the underlying mechanism of PGC-1α, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes with the potential to change the microglial function. Indeed, PGC-1α overexpression alters the gene expression profiles of microglia, this suggested that microglial PGC-1α might play an important role after ischemic stroke.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL21810
6 Samples
Download data: TXT
Series
Accession:
GSE124874
ID:
200124874
13.

CTCL and ATL cell lines, mir-150 transfected versus controls

(Submitter supplied) We examined the function of miR-150 in T-cell lymphomagenesis. We transfected GFP-control or GFP-miR-150 into several T-cell lymphoma lines and sought which genes were regulated by miR-150.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15496
8 Samples
Download data: TXT
Series
Accession:
GSE49308
ID:
200049308
14.

CD4 T cell response in AKI

(Submitter supplied) CD4+ T cells mediate the pathogenesis of ischemic and nephrotoxic acute kidney injury (AKI), as well as acute injury to other organs. However, the underlying mechanisms of CD4+ T cell-mediated pathogenesis are largely unknown. We therefore conducted unbiased RNA-sequencing to discover novel mechanistic pathways of kidney CD4+ T cells post-ischemia compared to normal mouse kidney. Unexpectedly, lipocalin-2 (Lcn2) gene, which encodes neutrophil gelatinase-associated lipocalin (NGAL) had the highest (~60)-fold increase. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: TXT
Series
Accession:
GSE139171
ID:
200139171
15.

Genome wide RNA expression profile of endometrial stromal cells stimulated by cAMP, and cAMP under PGC-1a-knockdown

(Submitter supplied) To know the role of PGC-1a in the change of mRNA expression during desidualization, we compared the mRNA expression profiles between cAMP-stimulation and cAMP-stimulation under PGC-1a-knockdown.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
3 Samples
Download data: XLSX
16.

A Gene Expression Profile in the Kidney After Cisplatin Treatment

(Submitter supplied) Clinical use of a major cancer chemotherapeutic agent, cisplatin, is restricted to dose-limiting renal toxicity. A transcriptomic approach enabled us to extract putative molecules including Pleckstrin homology-like domain, family A, member-3 (Phlda3) contributing to the renal injury. This study investigated the expression of Phlda3 and its regulatory role in tubular injury induced by cisplatin in vivo and in vitro. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: TXT
Series
Accession:
GSE35257
ID:
200035257
17.

Gpr97 exacerbates AKI via mediating Sema3A signaling

(Submitter supplied) We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish between the mice with renal IRI injury and sham-operated group.Expression of Gpr97 from this signature was quantified in the same kind of samples by real-time PCR, confirming the change pattern. By microarray analysis, we found that IR-induced Sema3A expression was significantly abolished by Gpr97 deficiency in mice
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
6 Samples
Download data: TXT
Series
Accession:
GSE108195
ID:
200108195
18.

TFEB-driven lysosomal biogenesis is pivotal for PGC1a-dependent renal stress resistance

(Submitter supplied) Because injured mitochondria can accelerate cell death through the elaboration of oxidative free radicals and other mediators, it is somewhat paradoxical that proliferator gamma coactivator 1-alpha (PGC1a), a stimulator of increased mitochondrial abundance, protects stressed renal cells instead of potentiating injury. Here we report that PGC1a’s induction of lysosomes via transcription factor EB (TFEB) may be pivotal for kidney protection. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: TXT
Series
Accession:
GSE126259
ID:
200126259
19.

Control of secreted protein gene expression and the mammalian secretome by the metabolic regulator PGC-1a

(Submitter supplied) Secreted proteins serve pivotal roles in the development of multicellular organisms, acting as structural matrix, extracellular enzymes and signal molecules. In this study we demonstrate, unexpectedly, that PGC-1α, a critical transcriptional co-activator of metabolic gene expression, functions to down-regulate expression of diverse genes encoding secreted molecules and extracellular matrix (ECM) components to modulate the secretome. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
4 Samples
Download data: CEL
Series
Accession:
GSE87100
ID:
200087100
20.

PGC-1a Provides a Transcriptional Framework for Synchronous Neurotransmitter Release from ParvalbuminPositive Interneurons

(Submitter supplied) PGC-1a is a master regulator for cell mitochondrial and metabolism function. In this experiment neurons were infected with a PGC-1a/GFP adenovirus to examine what genes were upregulated by over expression. Known targets related to mitochondrial health were confirmed while new neuron specific targets were discovered.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6884
6 Samples
Download data: TXT
Series
Accession:
GSE100341
ID:
200100341
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