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GSE43270
Homo sapiens
19 Downloadable Samples
Illumina HumanMethylation27 BeadChip (HumanMethylation27_270596_v.1.2), Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Genome-wide DNA methylation analysis of articular chondrocytes reveals a cluster of osteoarthritic patients.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 19 Downloadable Samples
- Illumina HumanMethylation27 BeadChip (HumanMethylation27_270596_v.1.2), Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
The aim of this study is to identify, for the first time, the genome-wide DNA methylation profiles of human articular chondrocytes from OA and healtly cartilage samples.
Publication Title
Genome-wide DNA methylation analysis of articular chondrocytes reveals a cluster of osteoarthritic patients.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 18 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The aim of this study was to identify differences in the NK-cell response towards Leishmania mexicana lipophosphoglycan (LPG) between patients with localized (LCL) and diffuse (DCL) cutaneous leishmaniasis through gene expression profiling, in an attempt to pinpoint alterations in the signaling pathways responsible for the NK-cell dysfunction in patients with DCL.
Publication Title
Down-Regulation of TLR and JAK/STAT Pathway Genes Is Associated with Diffuse Cutaneous Leishmaniasis: A Gene Expression Analysis in NK Cells from Patients Infected with Leishmania mexicana.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Transriptional profiling of white adipose tissue extracted from obese mice.
Publication Title
Loss of mitochondrial protease OMA1 alters processing of the GTPase OPA1 and causes obesity and defective thermogenesis in mice.
Sample Metadata Fields
Age, Specimen part
View Samples- Sus scrofa
- 26 Downloadable Samples
Illumina HiSeq 2000
Description
Identification of genes and causal mutations regulating growth and fatness traits in pig. Overall design: Transcriptome sequencing of 10 liver samples of two groups of divergent pigs for growth and fatness.
Publication Title
Using RNA-Seq SNP data to reveal potential causal mutations related to pig production traits and RNA editing.
Sample Metadata Fields
Sex, Age, Specimen part, Subject
View Samples- Sus scrofa
- 15 Downloadable Samples
- Affymetrix Porcine Genome Array (porcine)
Description
We studied the influence of the oleic acid content of the diet on adipose tissue transcriptome.
Publication Title
Dietary energy source largely affects tissue fatty acid composition but has minor influence on gene transcription in Iberian pigs.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 52 Downloadable Samples
- Illumina HiScanSQ
Description
Background & Aims. Glycine N-methyltransferase (GNMT) is an essential regulator of the total transmethylation flux in the mammalian liver. Distinct DNA methylation patterns are characteristic of liver development, hepatic de-differentiation and liver disease progression, processes in which the levels of GNMT decrease dramatically by mechanisms still poorly understood. Interestingly, putative binding sites for the microRNA miRNA-873-5p were identified in the 3´UTR of GNMT suggesting a potential role for miRNA-873-5p in GNMT regulation. Results. We have identified that the hepatic expression of miRNA-873-5p was increased in a cohort of cirrhotic and liver cancer patients associated with a down-regulation of GNMT levels. Moreover, during liver development, hepatic de-differentiation and fibrosis, the elevation of miRNA-873-5p coincided with the reduction of GNMT expression, indicating that miRNA-873-5p specifically targets the expression of GNMT. Under these circumstances, inhibition of miRNA-873-5p induced GNMT levels and decreased global CpG methylation and transmethylation flux. Indeed, reestablishment of GNMT expression by miRNA-873-5p inhibition reduced hepatocyte de-differentiation, and abolished completely the mortality produced after bile duct ligation as a result of decreased proinflamatory and profibrogenic markers. miRNA-873-5p knockdown-mediated antifibrotic effect was significantly blunted if its effect on GNMT was blocked. Conclusion. Taken together, our studies highlight the role of miRNA-873-5p as a key regulator of GNMT expression, paving the way for new therapeutical approaches in liver de-differentiation and fibrosis. Overall design: Genome-wide changes in gene Expression in mouse livers from BDL treated or not with anti-miR-873 were generated by RNAseq.
Publication Title
MiR-873-5p acts as an epigenetic regulator in early stages of liver fibrosis and cirrhosis.
Sample Metadata Fields
Age, Cell line, Treatment, Subject
View Samples- Sus scrofa
- 26 Downloadable Samples
- Affymetrix Porcine Genome Array (porcine)
Description
We studied the influence of genetic type (pure Iberian pigs vs crossbred with Duroc) on l.dorsi transcriptome
Publication Title
Longissimus dorsi transcriptome analysis of purebred and crossbred Iberian pigs differing in muscle characteristics.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 10 Downloadable Samples
- Illumina HiSeq 2000
Description
Precursor T-cell lymphoblastic neoplasms are aggressive haematological neoplasm that most often manifest with extensive marrow and blood affectation (T-cell acute lymphoblastic leukaemia or T-ALL) or less commonly as a thymic mass with limited bone marrow infiltration (T-cell lymphoblastic lymphoma or T-LBL). Here we show data from RNA-Seq in a sample series of T-LBL from Spanish patients.The goal was to determine the levels of expression of coding genes and microRNAs, and to identify all genetic variants including SNVs, indels, and fusion transcripts. Overall design: Expression data were determined by comparson of each tumour sample with two control thymuses (404 and 405). Genetic variants were determined by comparison of tumour sequences with canonical ENSEMBL normal-references of each gene.
Publication Title
RNA-Seq reveals the existence of a CDKN1C-E2F1-TP53 axis that is altered in human T-cell lymphoblastic lymphomas.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The identification of inflammatory bowel disease (IBD) susceptibility genes by genome-wide association has linked this pathology to autophagy, a lysosomal degradation pathway that is crucial for cell and tissue homeostasis. Here, we describe autophagin-1 (ATG4B) as an essential protein in the control of inflammatory response during experimental colitis. In this pathological condition, ATG4B protein levels increase paralleling the induction of autophagy. Moreover, ATG4B expression is significantly reduced in affected areas of the colon from IBD patients. Consistently, atg4b-/- mice present Paneth cell abnormalities, as well as an increased susceptibility to DSS-induced colitis. Atg4b-deficient mice exhibit significant alterations in proinflammatory cytokines and mediators of the immune response to bacterial infections, which are reminiscent of those found in patients with Crohns disease or ulcerative colitis. Additionally, antibiotic treatments and bone marrow transplantation from wild-type mice reduced colitis in atg4b-/- mice. Taken together, these results provide additional evidence on the importance of autophagy in intestinal pathologies and describe ATG4B as a novel protective protein in inflammatory colitis. Finally, we propose that Atg4b-null mice are a suitable model for in vivo studies aimed at testing new therapeutic strategies for intestinal diseases associated with autophagy deficiency
Publication Title
ATG4B/autophagin-1 regulates intestinal homeostasis and protects mice from experimental colitis.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples