Embryonic retinal development Overall design: Mouse retinas at different embryonic developmental stages were isolated and mRNA expression was determined by RNA sequencing
Programmed mitophagy is essential for the glycolytic switch during cell differentiation.
Specimen part, Cell line, Subject
View SamplesRecently, it was described that mammalian cells are able to eliminate those with relative lower Myc levels in the epiblast through cell competition. We have described that cardiomyocytes during heart development are also able to complete eliminating cells with lower Myc levels. We have also shown that adult cardiomyocytes respond in the same way over long periods of time when cell competition is induced by overexpressing Myc in a mosaic fashion. We therefore have developed an RNASeq assay to further understand the mechanism of elimination of WT cells and the effect of mild Myc overexpression in cardiomyocytes. Overall design: Myc overexpression in a mosaic fashion in adult cardiomyocytes, 2 hearts were analyzed and two wild type littermates were used as controls
Cell competition promotes phenotypically silent cardiomyocyte replacement in the mammalian heart.
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View SamplesWe used microarray analysis to profile the function of TCF7L1 in human embryonic stem cells.
TCF7L1 suppresses primitive streak gene expression to support human embryonic stem cell pluripotency.
Cell line
View SamplesWe used microarray analysis to profile the function of TCF7L1 in human embryonic stem cells.
TCF7L1 suppresses primitive streak gene expression to support human embryonic stem cell pluripotency.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Expansion on stromal cells preserves the undifferentiated state of human hematopoietic stem cells despite compromised reconstitution ability.
Specimen part, Cell line
View SamplesOne of the long-standing goals in the field has been to establish a culture system that would allow maintenance of HSC properties ex vivo. In the absence of such system, the ability to model human hematopoiesis in vitro has been limited, and there has been little progress in the expansion of human HSCs for clinical application. To that end, we defined a mesenchyml stem cell co-culture system for expansion of clonally multipotent human HSPCs that are protected from apoptosis and immediate differentiation, and retain the HSPC phenotype. By performing a genome-wide gene expression analysis of purified HSPCs isolated at different stages of co-culture, we asked at the molecular level, to what degree hematopetic stem cell properties can be preserved during culture. This temporal gene expression data from in vivo derived- and ex vivo expanded human HSPCs will serve as a resource to identify novel regulatory pathways that control HSC properties, and to develop clinically applicable protocols for HSC expansion.
Expansion on stromal cells preserves the undifferentiated state of human hematopoietic stem cells despite compromised reconstitution ability.
Specimen part
View SamplesOne of the long-standing goals in the field has been to establish a culture system that would allow maintenance of HSC properties ex vivo. In the absence of such system, the ability to model human hematopoiesis in vitro has been limited, and there has been little progress in the expansion of human HSCs for clinical application. To that end, we defined a mesenchymal stem cell co-culture system based on a monoclonal OP9 stromal cell line (OP9M2), for expansion of clonally multipotent human HSPCs that were protected from apoptosis and immediate differentiation, and retained the HSPC phenotype. To identify the supportive mechanisms, we performed a genome-wide gene expression analysis of OP9M2 stromal cells and compared the expression to a non-supportive stomal line (BFC012). This co-culture system provides a new, well-defined platform for studying mechanisms involved in HSC-niche interactions and protection of critical HSC properties ex vivo.
Expansion on stromal cells preserves the undifferentiated state of human hematopoietic stem cells despite compromised reconstitution ability.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-Nuclear Lamina Interactions Regulate Cardiac Stem Cell Lineage Restriction.
Specimen part, Cell line, Treatment
View SamplesProgenitor cells require coordinated expression of lineage-specific programs, and the nuclear lamina has emerged as an important scaffold for organizing chromatin in many cell types. These transcriptome profiling experiments accompany a study focused on defining nuclear organization changes during cardiac development. This dataset defines gene expression changes induced by Hdac3 deletion during early stages of cardiogenesis, modeled using ESC differentiation assays.
Genome-Nuclear Lamina Interactions Regulate Cardiac Stem Cell Lineage Restriction.
Cell line, Treatment
View SamplesTumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-B2 (NF-B2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family). This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo. We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling. As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells. This analysis should identify genes that are important in B cell survival.
TRAF2 and TRAF3 signal adapters act cooperatively to control the maturation and survival signals delivered to B cells by the BAFF receptor.
Sex, Age
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