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Xenopus laevis
5 Downloadable Samples
Affymetrix Xenopus laevis Genome Array (xenopuslaevis)
Description
Analysis of epithelial explants injected with the intracellular domain of Notch (ICD) to block the formation of multi-ciliate cells, either alone or along with FoxJ1. FoxJ1 misexpression leads to the induction fo ectopic cilia in Xenopus laevis epithelia. Results show which genes are affected by FoxJ1 during the induction of ectopic cilia.
Publication Title
The forkhead protein Foxj1 specifies node-like cilia in Xenopus and zebrafish embryos.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Total RNA was extracted from apratoxin A or vehicle treated HT29 cells using the RNeasy Mini Kit (Qiagen). Probe values from CEL files were condensed to probe sets using Rosetta Resolver software. Resolver ANOVA analysis was then performed between groups.
Publication Title
A functional genomics approach to the mode of action of apratoxin A.
Sample Metadata Fields
No sample metadata fields
View Samples- Danio rerio
- 12 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Conditional expression of dominant-negative HIF1a in zebrafish cardiomyocytes severely inhibits heart regeneration. To understand more about the mechanism, we performed microarray analysis of wildtype regenerating zebrafish and dnHIF1a regenerating zebrafish to determine which genes are regulated by hypoxia/HIF1a.
Publication Title
Hypoxia induces myocardial regeneration in zebrafish.
Sample Metadata Fields
Specimen part, Treatment
View Samples
GSE17993- Danio rerio
- 15 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Ischemic cardiopathy is the leading cause of death in the world, for which efficient regenerative therapy is not currently available. In mammals, after a myocardial infarction episode, the damaged myocardium is replaced by scar tissue featuring collagen deposition and tissue remodelling with negligible cardiomyocyte proliferation. Zebrafish, in contrast, display an extensive regenerative capacity as they are able to restore completely lost cardiac tissue after partial ventricular amputation. Due to the lack of genetic lineage tracing evidence, it is not yet clear if new cardiomyocytes arise from existing contractile cells or from an uncharacterised set of progenitors cells. Nonetheless, several genes and molecules have been shown to participate in this process, some of them being cardiomyocyte mitogens in vitro. Though questions as what are the early signals that drive the regenerative response and what is the relative role of each cardiac cell in this process still need to be answered, the zebrafish is emerging as a very valuable tool to understand heart regeneration and devise strategies that may be of potential value to treat human cardiac disease. Here, we performed a genome-wide transcriptome profile analysis focusing on the early time points of zebrafish heart regeneration and compared our results with those of previously published data. Our analyses confirmed the differential expression of several transcripts, and identified additional genes the expression of which is differentially regulated during zebrafish heart regeneration. We validated the microarray data by conventional and/or quantitative RT-PCR. For a subset of these genes, their expression pattern was analyzed by in situ hybridization and shown to be upregulated in the regenerating area of the heart. The specific role of these new transcripts during zebrafish heart regeneration was further investigated ex vivo using primary cultures of zebrafish cardiomyocytes and/or epicardial cells. Our results offer new insights into the biology of heart regeneration in the zebrafish and, together with future experiments in mammals, may be of potential interest for clinical applications.
Publication Title
Transcriptomics approach to investigate zebrafish heart regeneration.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The generation of induced pluripotent stem (iPS) cells 1-4 has spawned unprecedented opportunities for investigating the molecular logic that underlies cellular pluripotency and reprogramming, as well as for obtaining patient-specific cells for future clinical applications. However, both prospects are hampered by the low efficiency of the reprogramming process. Here, we show that juvenile human primary keratinocytes can be efficiently reprogrammed to pluripotency by retroviral transduction with Oct4, Sox2, Klf4 and c-Myc. Keratinocyte-derived iPS (KiPS) cells appear indistinguishable from human embryonic stem (hES) cells in colony morphology, growth properties, expression of pluripotency-associated transcription factors and surface markers, as well as in vitro and in vivo differentiation potential. Notably, keratinocyte reprogramming to pluripotency is, at least, 100-fold more efficient and 2-fold faster than that of fibroblasts. This increase in reprogramming efficiency allowed us to expand the practicability of the technology and to generate KiPS cells from single plucked hairs from adult individuals.
Publication Title
Efficient and rapid generation of induced pluripotent stem cells from human keratinocytes.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The events regulating human preimplantation development are still largely unknown, due to scarcity of material, ethical and legal limitations, and lack of reliable techniques to faithfully amplify the transcriptome of a single cell. Nonetheless, knowledge in human embryology is gathering renewed interest due to its close relationship with both stem cell biology and epigenetic reprogramming to pluripotency, and their centrality to regenerative medicine. Using carefully timed genome-wide transcript analyses on single oocytes and embryos, the analysis of the data allowed us to uncover a series of successive waves of embryonic transcriptional initiation which start as early as the 2 cell stage. In addition, we identified hierarchical activation of genes involved in the regulation of pluripotency. Finally, we developed HumER, a free database of human preimplantation human development gene expression to serve the scientific community. Importantly, our work links early transcription in the human embryo with the correct execution of the pluripotency program later in development, and paves the way for the identification of factors to improve epigenetic reprogramming.
Publication Title
Waves of early transcriptional activation and pluripotency program initiation during human preimplantation development.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Parthenogenetic stem cells were derived from parthenotes, then differentiated to mesenchymal stem cells. These were further reprogrammed to induced pluripotent stem cells, which were finally differentiated to secondary mesenchymal stem cells.
Publication Title
Accumulation of instability in serial differentiation and reprogramming of parthenogenetic human cells.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
Illumina HiSeq 2500
Description
we identify several downstream targets that are under control of miR25/93 cluster Overall design: examination of global changes in mRNAs in two different lines
Publication Title
miR-25/93 mediates hypoxia-induced immunosuppression by repressing cGAS.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 2000, Illumina HiSeq 2500
Description
Premature senescence-associated functional decay and neoplastic transformation of transplanted human stem cells or their derivatives represent two major roadblocks for regenerative medicine. Cellular senescence acts as a major mechanism antagonizing neoplastic transformation, and stem cells evading senescence are prone to oncogenic transformation. So far it is unknown whether there is any genetic code, rewriting of which can simultaneously brake cellular senescence and oncogenic transformation programs. Here, we identify a single nucleotide in human genome(target on the transcription factor NRF2) as a candidate code, switch of which blocks both senescence and transformation pathways. Genetic modification stabilizes the wild type human mesenchymal stem cells (hMSCs) at a “sustainably younger” state. More importantly, the same genetic manipulation endows hMSCs with the ability of counteracting oncogenic transformation. Our study thus provides the first proof-of-concept of genetic enhancement of human stem cells, a strategy holding potential to generate superior and safer stem cell materials for cell replacement therapy. Overall design: RNA-seq of MSCs-NRF2 +/+_EP, MSCs-NRF2 AG/AG_EP, MSCs-NRF2 +/+_LP, MSCs-NRF2 AG/AG_LP, TMSCs-NRF2 +/+ and TMSCs-NRF2 AG/AG.
Publication Title
Genetic enhancement in cultured human adult stem cells conferred by a single nucleotide recoding.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Since the initial discovery that OCT4, SOX2, KLF4 and c-MYC overexpression sufficed for the induction of pluripotency in somatic cells, methodologies replacing the original factors have enhanced our understanding of the reprogramming process. However, unlike in mouse, OCT4 has not been replaced successfully during reprogramming of human cells. Here we report on a strategy to do so. Through a combination of transcriptome and bioinformatic analysis we have identified factors previously characterized as being lineage specifiers that are able to replace OCT4 and SOX2 in the reprogramming of human fibroblasts. Our results show that is possible to replace OCT4 and SOX2 simultaneously with alternative lineage specifiers in the reprogramming of human cells. At a broader level, they also support a model in which counteracting lineage specification networks underlie the induction of pluripotency,
Publication Title
Reprogramming of human fibroblasts to pluripotency with lineage specifiers.
Sample Metadata Fields
Specimen part
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