CD34+ fraction of cord blood (CB) cells can be reprogrammed on pronectinF-coated dish in serum free medium using Sendai virus (SeV) vector carrying reprogramming factors OCT3/4, SOX2, KLF4 and c-MYC. human ES cell-like colonies came to merge around 18 days after SeV infection on pronectin-coated dish in human ES cell medium supplemented with bFGF under normoxic culture (20% O2). After passages, dish like-shape colonies were seeded on pronectinF-coated 96 well-plate in a single cell and cultured in N2B27 based medium supplemented with LIF, FK, MAPKi, GSKi in hypoxic culture condition (5% O2) for cloning purpose. Emerged dome shape colonies were collected and cultured in human ES cell medium supplemented with bFGF under normoxic culture (20% O2) again. Dish shape and human ES cell-like colonies derived from single cell were picked up for further appraisal of reprogrammed cells such as expression of pluriotencyrelated molecules. Reprogrammed cells can be maintained for more than 20 passages without differentiation.
Generation of virus-free induced pluripotent stem cell clones on a synthetic matrix via a single cell subcloning in the naïve state.
Specimen part
View SamplesWe investigated that gene expression profile of generated human iPS cells from cord blood cells using temperature sensitive sendai-virus vector.
Efficient generation of transgene-free human induced pluripotent stem cells (iPSCs) by temperature-sensitive Sendai virus vectors.
Specimen part
View SamplesWe show that Retinal pigment epithelium (RPE) secreted-factor, pigment epithelium derived factor (PEDF) secreted/derived from primary or iPSC-derived retinal pigment epithelium (RPE)RPE, dramatically inhibitsed the cell growth of iPSCs. PEDF was detected abundantly in culture supernatant media of primary and iPSC-derived RPE. We examined the gene expression in primary RPE and iPS-derived RPE.
No associated publication
Specimen part
View SamplesThis goal of this study was to investigate the gene expression effect of disease associated polymorphisms in the endoplasmic reticulum aminopeptidase genes ERAP1 and ERAP2. The enzymes ERAP1 and ERAP2, encoded on chromosome 5q15, function by trimming endogenously derived peptides for human leukocyte antigen (HLA) mediated presentation to the immune system. Polymorphisms in ERAP1 and/or ERAP2 have been observed in several immune-mediated diseases with specific HLA associations, implicating altered peptide handling and presentation as a prerequisite for immune autoreactivity. Evidence for the elevated expression or altered transcriptional profile of these genes in diseases characterised by immune autoreactivity provides grounds for the development of aminiopeptidase inhibitors for the therapeutic treatment of such conditions.
No associated publication
Sex, Age, Specimen part, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Jarid1b targets genes regulating development and is involved in neural differentiation.
Specimen part
View SamplesThe H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) is dispensable for embryonic stem cell (ESC) self-renewal, but essential for ESC differentiation along the neural lineage. During neural differentiation, Jarid1b depleted ESCs fail to efficiently silence lineage-inappropriate genes, specifically stem and germ cell genes. Our results delineate an essential role for Jarid1b-mediated transcriptional control during ESC differentiation.
Jarid1b targets genes regulating development and is involved in neural differentiation.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
No sample metadata fields
View SamplesEmbryonic development is tightly regulated by transcription factors and chromatin-associated proteins. H3K4me3 is associated with active transcription and H3K27me3 with gene repression, while the combination of both keeps genes required for development in a plastic state. Here we show that deletion of the H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) results in major neonatal lethality due to respiratory failure. Jarid1b knockout embryos have several neural defects including disorganized cranial nerves, defects in eye development and increased incidences of exencephaly. Moreover, in line with an overlap of Jarid1b and Polycomb targets genes, Jarid1b knockout embryos display homeotic skeletal transformations typical for Polycomb mutants. Genome-wide analysis demonstrated that normally inactive genes encoding developmental regulators acquire aberrant H3K4me3 in early Jarid1b knockout embryos. H3K4me3 accumulates as embryonic development proceeds, leading to increased expression of neural master regulators in knockouts. Taken together, these results suggest that Jarid1b contributes to mouse development by protecting developmental genes from inappropriate acquisition of active histone modifications.
The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3.
No sample metadata fields
View SamplesDownsream of GRID2 in the mouse cerebellum.
Altered Actions of Memantine and NMDA-Induced Currents in a New Grid2-Deleted Mouse Line.
Sex, Age
View SamplesChronic obstructive pulmonary disease is a smoking-related disease that lacks effective therapies due partly to the poor understanding of disease pathogenesis. The aim of this study was to identify molecular pathways which could be responsible for the damaging consequences of smoking. To do this, we employed recently described bioinformatic methods to analyze differences in global gene expression, which we then related to the pathological changes induced by cigarette smoke (CS). Sprague-Dawley rats were exposed to whole-body CS for 1 day and for various periods up to 8 months.
Comprehensive gene expression profiling of rat lung reveals distinct acute and chronic responses to cigarette smoke inhalation.
Sex, Specimen part
View Samples