Pluripotency is the differentiation capacity of particular cells exhibited in the early embryo in vivo and embryonic stem (ES) cells have been shown to originate from the inner cell mass (ICM) of an E3.5 blastocyst. Although the potential for ES cells to differentiate into the three germ layers is equated to ICM cells, they differ in the ability to maintain the capacity for self-renewal. Despite several studies on the maintenance of ES cells in the ground state of pluripotency, the precise mechanism of conversion from the ICM to the ES cell remains unclear. Here , we have examined the cell characteristics and expression profile within the intermediate stages of ES cell derivation from the ICM. Gene clustering and ontology (GO) analyses showed a significant change in the expression of epigenetic modifiers and DNA methylation-related genes in the intermediate stages. We have proposed that an epithelial-to-mesenchymal transition (EMT) blockage is required during derivation of mouse ES cells from E3.5 blastocysts. This study suggests a novel mechanistic insight into ES cell derivation and provides a time-course transcriptome profiling resource for the dissection of gene regulatory networks that underlie the transition from ICM to ES cells.
Blockage of the Epithelial-to-Mesenchymal Transition Is Required for Embryonic Stem Cell Derivation.
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View SamplesIn this study we have analyzed the global gene expression of nave mouse embryonic stem cells in different culture conditions including R2i (PD0325901+SB431542), 2i (PD0325901+CHIR99021), and also PD0325901+LIF and SB431542+LIF to show the similarities and differences between the conditions in maintaining pluripotency.
Inhibition of TGFβ signaling promotes ground state pluripotency.
Specimen part, Cell line
View SamplesWe used microarrays to investigate gene expression from peritoneal macrophages associated with Ninjurin1 expression.
Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions.
Sex
View SamplesNTHi bacteria or saline were inoculated into the middle ears of mice. Mice were sacrificed at various times to monitor the course of infection.
The transcriptome of a complete episode of acute otitis media.
Specimen part, Treatment, Time
View SamplesCML stem cells (CMLSCs) and normal hematopoietic stem cells (HSCs) display the same set of surface markers (CD34+CD38-CD90+CD45RA-), making it infeasible to separate these two populations within the same sample. To overcome this challenge, and to minimize variations in gene expression due to individual variation, here we perform single-cell RNA-seq to compare expression profiles of CMLSCs and HSCs isolated from the same patient. We captured ~600 HSCs (CD34+CD38-CD90+CD45RA-) (~200 from each of three CML patient samples), separated them into CMLSCs (BCR-ABL+) or normal HSCs (BCR-ABL-) based on the presence of the BCR-ABL transcript, and performed paired-end deep sequencing. Typically, we obtained ~2.5 million mapped reads (>70% average mapping efficiency) and detected ~5,000 genes (transcript per million [TPM]>1) per cell. Despite the heterogeneity of the gene expression pattern, we were able to identify genes that were significantly more highly expressed in CMLSCs than in normal HSCs. Notably, among these genes are two cell surface markers, CD33 and CD47, that could potentially be used to distinguish CMLSCs from normal HSCs. We also found genes, such as PIM2, that could be targeted for CML therapy using available small molecule inhibitors. Overall design: Hematopoietic stem cell population from three chronic phase CML patients with no detectable BCR-ABL mutation.
Prosurvival kinase PIM2 is a therapeutic target for eradication of chronic myeloid leukemia stem cells.
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View SamplesAnalysis of hormone effects on irradiated LBNF1 rat testes, which contain only somatic cells except for a few type A spermatgogonia. Rats were treated for 2 weeks with either sham treatment (group X), hormonal ablation (GnRH antagonist and the androgen receptor antagonist flutamide, group XAF), testosterone supplementation (GnRH antagonist and testosterone, group XAT), and FSH supplementation ((GnRH antagonist, androgen receptor antagonist, and FSH, group XAFF). Results provide insight into identifying genes in the somatic testis cells regulated by testosterone, LH, or FSH.
Changes in gene expression in somatic cells of rat testes resulting from hormonal modulation and radiation-induced germ cell depletion.
Specimen part, Treatment
View SamplesAnalysis of LBNF1 rat testes from controls, containing both somatic and all germ cell types and from irradiated rats in which all cells germ cells except type A spermatgogonia are eliminated. Results provide insight into distinguishing germ and somatic cell genes and identification of somatic cell genes that are upregulated after irradiation.
Changes in gene expression in somatic cells of rat testes resulting from hormonal modulation and radiation-induced germ cell depletion.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epigenetic regulator Smchd1 functions as a tumor suppressor.
Specimen part
View SamplesSmchd1 appears to act as a tumour suppressor in the transformed fibroblast model. We find gene expression differences are most pronounced in the transformed MEFs. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis.
Epigenetic regulator Smchd1 functions as a tumor suppressor.
Specimen part
View SamplesExpression data from 22 human myotubes (7 healthy controls, 4 Dysferlinopathy (DYSF), 4 Caveolinopathy 3 (CAV3), 4 Facioscapulohumeral muscular dystrophy(FSHD) and 3 Four and a half LIM 1 protein deficiency FHL1).cDNA microarray data showed that cyclin A1 levels are specifically elevated in FSHD vs. other muscular disorders such as CAV3, DYSF, FHL1 and healthy control. Data could be confirmed with RT-PCR and Western blot analysis showing up-regulated levels of cyclin A1 also on the protein level.
Altered expression of cyclin A 1 in muscle of patients with facioscapulohumeral muscle dystrophy (FSHD-1).
Age, Specimen part, Disease, Disease stage
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