Forkhead BoxO (FoxO) transcription factors expressed in adult skeletal muscle promote muscle atrophy during various catabolic conditions. We have identified the genome wide target genes and biological networks regulated by FoxO in skeletal muscle during Colon-26 (C-26) cancer cachexia.
Genome-wide identification of FoxO-dependent gene networks in skeletal muscle during C26 cancer cachexia.
Specimen part, Disease, Disease stage, Treatment
View SamplesThe activation signaling of transcription factor nuclear factor-kB (NF-kB) plays central role for immune system. One of key kinase mediating this pathway is TAK1 in adaptive and innate immunity.
Positive feedback within a kinase signaling complex functions as a switch mechanism for NF-κB activation.
Sex, Specimen part
View SamplesHuman genome-wide Affymetrix GeneChip arrays were used to compare the levels of gene expression in the peripheral blood mononuclear cells (PMBCs) of male patients with post-viral chronic fatigue (n=8) and male healthy control subjects (n=7). Patients and healthy subjects differed significantly in the level of expression of 366 genes. Analysis of the differentially expressed genes indicated functional implications in immune modulation, oxidative stress and apoptosis. Prototype biomarkers were identified on the basis of differential levels of gene expression and possible biological significance. Differential expression of key genes identified in this study offer an insight into the possible mechanism of chronic fatigue following infection. The representative biomarkers identified in this research appear promising as potential biomarkers for diagnosis and treatment.
A gene signature for post-infectious chronic fatigue syndrome.
No sample metadata fields
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An integrative genomic approach in oesophageal cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's oesophagus, which regulates NF-kappaB activation and cytokine levels.
No sample metadata fields
View SamplesThe involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barretts metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisons with data derived from gene expression studies of Barretts esophagus and associated adenocarcinoma.
An integrative genomic approach in oesophageal cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's oesophagus, which regulates NF-kappaB activation and cytokine levels.
No sample metadata fields
View SamplesThe involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barretts metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barretts esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line.
An integrative genomic approach in oesophageal cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's oesophagus, which regulates NF-kappaB activation and cytokine levels.
No sample metadata fields
View SamplesThis study utilise the examination of normal gastro-intestinal tissues to determine a tissue specific signal for use in deriving the intestinal signature of intestinal metaplasias of the oesophagus. Normal oesophageal, colonic and duodenal tissue biopsies were taken after informed consent and RNA was extracted following histological examination of adjacent tissues for normal aperaing mucosa.
The characterization of an intestine-like genomic signature maintained during Barrett's-associated adenocarcinogenesis reveals an NR5A2-mediated promotion of cancer cell survival.
Specimen part
View SamplesThe objective of this study was the assessment of transcriptional dysregulation in particular with regard to B-cell differentiation factors. Most studies focus on cross-section analyses of various leukemia subtypes to identify differentially regulated genes lacking suitable reference models. Here we applied comparative intraindividual transcriptome analysis of B-precursor ALL of childhood, which introduces a side-by-side analysis of leukemic cells and matched normal lymphoblasts from the same individual in complete continuous remission after the end of re-induction therapy. This approach reduces noise by eliminating interindividual variability.
Aberrant ZNF423 impedes B cell differentiation and is linked to adverse outcome of ETV6-RUNX1 negative B precursor acute lymphoblastic leukemia.
Specimen part, Subject
View Samplesgamma delta intraepithelial lymphocytes were isolated from the colons of DSS-treated and untreated mice. Total RNAs were isolated and compared by Affymetrix DNA microarray.
Reciprocal interactions between commensal bacteria and gamma delta intraepithelial lymphocytes during mucosal injury.
No sample metadata fields
View SamplesThe goal of the microarray experiment was to do a head-to-head comparison of the U1 Adaptor technology with siRNA in terms of specificity at the genome-wide level. U1 Adaptors represent a novel gene silencing method that employs a mechanism of action distinct from antisense and RNA interference (RNAi). The U1 Adaptor is a bifunctional oligonucleotide having a Target Domain that is complementary to a site in the target gene's terminal exon and a U1 Domain that binds to the U1 small nuclear RNA (snRNA) component of the U1 small nuclear ribonucleoprotein (U1 snRNP) splicing factor. Tethering of U1 snRNP to the target pre-mRNA inhibits 3' end processing (i.e., polyA tail addition) leading to degradation of that RNA species within the nucleus thereby reducing mRNA levels. We demonstrate that U1 Adaptors can specifically inhibit both reporter and endogenous genes. Further, targeting the same gene either with multiple U1 Adaptors or with U1 Adaptors and small interfering RNAs (siRNAs), strongly enhances gene silencing, the latter as predicted from their distinct mechanisms of action. Such combinatorial targeting requires lower amounts of oligonucleotides to achieve potent silencing.
Gene silencing by synthetic U1 adaptors.
No sample metadata fields
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