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GSE115247
Mus musculus
5 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
We describe here an interrupted reprogramming strategy to generate "induced Progenitor-Like (iPL) cells" from Alveolar Epithelial Type II (AEC-II) cells. A carefully defined period of transient expression of reprogramming factors (Oct4, Sox2, Klf4 and c-Myc; OSKM) is able to rescue the limited in vitro clonogenic capacity of AEC-II cells, potentially by activation of a bipotential progenitor-like state.
Publication Title
Interrupted reprogramming of alveolar type II cells induces progenitor-like cells that ameliorate pulmonary fibrosis.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Comparison of the changes in mitochondrial gene expression of cells in which extracellular growth factors and/or mitogens have been added.
Publication Title
Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis.
Sample Metadata Fields
Specimen part
View Samples- Pseudomonas aeruginosa
- 6 Downloadable Samples
- Affymetrix Pseudomonas aeruginosa Array (paeg1a)
Description
Analysis of a SigX knockout mutant of Pseudomonas aeruginosa H103 strain in LB.
Publication Title
The absence of SigX results in impaired carbon metabolism and membrane fluidity in Pseudomonas aeruginosa.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 10 Downloadable Samples
Affymetrix Murine Genome U74A Array (mgu74a), Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2), Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Autoregulation of Th1-mediated inflammation by twist1.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2), Affymetrix Murine Genome U74A Array (mgu74a)
Description
Gene expression profiling of repeatedly activated compared to recently activated Th1 cells to identify genes that play a role in chronic inflammatory disorders and may qualify as diagnostic or therapeutic targets;
Publication Title
Autoregulation of Th1-mediated inflammation by twist1.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
The basic helix-loop-helix transcriptional repressor twist1, as an antagonist of nuclear factor B (NF-B)-dependent cytokine expression, is involved in the regulation of inflammation-induced immunopathology. We could show that twist1 is expressed by activated T helper (Th) 1 effector memory cells. Induction of twist1 in Th cells is dependent on NF-B, nuclear factor of activated T cells (NFAT), and interleukin (IL)-12 signaling via signal transducer and activator of transcription (STAT) 4. Expression of twist1 is transient following T-cell receptor engagement, and increases upon repeated stimulation of Th1 cells. Imprinting for enhanced twist1 expression is characteristic of repeatedly restimulated effector memory Th cells and thus of the pathogenic memory Th cells of chronic inflammation. Th lymphocytes from the inflamed joint or gut tissue of patients with rheumatic diseases, Crohns disease or ulcerative colitis express high levels of twist1. Expression of twist1 in Th1 lymphocytes limits the expression of the cytokines interferon-, IL-2 and tumor necrosis factor-, and ameliorates Th1-mediated immunopathology in delayed-type hypersensitivity and antigen-induced arthritis. In order to identify the effect of twist1 expression on the function of Th cells, twist1 was ectopically expressed and the transcriptome was compared to empty-virus infected control cells. In addition, this experiment allows for the identification of genes regulated by the transcription factor twist1.
Publication Title
Autoregulation of Th1-mediated inflammation by twist1.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 14 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
The intestinal epithelium is continuously renewed by a pool of intestinal stem cells expressing Lgr5. We show that deletion of the key autophagy gene Atg7 affects the survival of Lgr5+ intestinal stem cells. Mechanistically, this involves defective DNA repair, oxidative stress, and altered interactions with the microbiota. This study highlights the importance of autophagy in maintaining the integrity of intestinal stem cells.
Publication Title
Essential role for autophagy protein ATG7 in the maintenance of intestinal stem cell integrity.
Sample Metadata Fields
Specimen part
View Samples- Drosophila melanogaster
- 24 Downloadable Samples
Illumina HiSeq 2500
Description
Effect of LUBEL catalytic dead mutation in immune response Overall design: Mutation was introduced in the LUBEL catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and their transcriptome was compared in control (sample 23930 to 23941) and e.coli pricked samples (sample 28984 to 28995).
Publication Title
Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Drosophila melanogaster
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
Effect of LUBEL catalytic dead mutation upon Heastshock Overall design: Mutation was introduced in CG11321 catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and transcriptome was compared in untreated and heatshocked samples
Publication Title
Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.
Sample Metadata Fields
Treatment, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The cytosolic protein Sharpin is as a component of the linear ubiquitin chain assembly complex (LUBAC), which regulates NF-B signaling in response to specific ligands. Its inactivating mutation in Cpdm (chronic proliferative dermatitis mutation) mice causes multi-organ inflammation, yet this phenotype is not transferable into wildtype mice by hematopoietic stem cell transfer. Recent evidence demonstrated that Cpdm mice additionally display low bone mass, but the cellular and molecular causes of this phenotype remained to be established. Here we have applied non-decalcified histology together with cellular and dynamic histomorphometry to perform a thorough skeletal phenotyping of Cpdm mice. We show that Cpdm mice display trabecular and cortical osteopenia, solely explained by impaired bone formation, whereas osteoclastogenesis is unaffected. We additionally found that Cpdm mice display a severe disturbance of articular cartilage integrity in the absence of joint inflammation, supporting the concept that Sharpin-deficiency affects mesenchymal cell differentiation. Consistently, Cpdm mesenchymal cells displayed reduced osteogenic capacitiy ex vivo, yet this defect was not associated with impaired NF-B signaling. A molecular comparison of wildtype and Cpdm bone marrow cell populations further revealed that Cpdm mesenchymal cells produce higher levels of Cxcl5 and lower levels of IL1ra. Collectively, our data demonstrate that skeletal defects of Cpdm mice are not caused by chronic inflammation, but that Sharpin is as a critical regulator of mesenchymal cell differentiation and gene expression. They additionally provide an alternative molecular explanation for the inflammatory phenotype of Cpdm mice and the absence of disease transfer by hematopoetic stem cell transplantation.
Publication Title
Sharpin Controls Osteogenic Differentiation of Mesenchymal Bone Marrow Cells.
Sample Metadata Fields
Specimen part
View Samples