Analysis of gene expression levels from oral tumor and normal tissue. The purpose of this experiment was to compare profiles of gene expression between tumor and negative margin tissue from matched patient samples.
Tumor transcriptome sequencing reveals allelic expression imbalances associated with copy number alterations.
Specimen part
View SamplesMED23, a subunit of the Mediator coactivator complex, is important for the expression of a subset of MAPK/ERK pathway-dependent target genes; however, the genes in this subset varies between cell types. MAPK/ERK pathway-dependent processes are essential for T-cell development and function, but whether MED23 has a role in this context is unknown. We generated Med23 conditional knockout mice and induced Med23 deletion in early T cell development using the lineage specific Lck-Cre transgene. While the total cell number and distribution of cell populations in the thymuses of Med23flox/flox;Lck-Cre mice were essentially normal, MED23 null T-cells failed to efficiently populate the peripheral lymphoid organs. MED23 null thymocytes displayed decreased expression of the MAPK/ERK-responsive genes Egr1, Egr2, as well as of the membrane glycoprotein Cd52 (CAMPATH-1). MED23 null CD4 single-positive thymocytes also showed decreased expression of KLF2 (LKLF), a T cell master regulatory transcription factor. Indeed, similarities between the phenotypes of mice lacking MED23 or KLF2 in T-cells suggest that KLF2 deficiency in MED23 null T-cells is one of their key defects. Mechanistic experiments using MED23 null MEFs further suggest that MED23 is required for full activity of the MAPK-responsive transcription factor MEF2, which has previously been shown to mediate Klf2 expression. In summary, our data indicate that MED23 has critical roles in enabling T-cells to populate the peripheral lymphoid organs, possibly by potentiating MEF2-dependent expression of the T-cell transcription factor KLF2.
T-cells null for the MED23 subunit of mediator express decreased levels of KLF2 and inefficiently populate the peripheral lymphoid organs.
Sex, Specimen part
View SamplesPurpose: We applied cDNA molecule counting using unique molecular identifiers combined with high-throughput sequencing to study the transcriptome of individual mouse embryonic stem cells, with spike-in controls to monitor technical performance. We further examined transcriptional noise in the embryonic stem cells. Overall design: One 96-well plate of single-stranded cDNA libraries generated from 96 single R1 mouse embryonic stem cells sequenced on two lanes, and one 96-well plate of the same libraries further amplified by 9 PCR cycles sequenced on one lane.
Quantitative single-cell RNA-seq with unique molecular identifiers.
No sample metadata fields
View SamplesIn order to identify the gene targets of frequently altered chromosomal regions in retinoblastoma, a meta-analysis of genome-wide copy number alterations studies on primary retinoblastoma tissue and retinoblastoma cell lines was performed. Published studies were complemented by copy number and gene expression analysis on primary and cell line samples of retinoblastoma. This dataset includes the gene expression data of the retinoblastoma cell lines
A Meta-Analysis of Retinoblastoma Copy Numbers Refines the List of Possible Driver Genes Involved in Tumor Progression.
Specimen part, Cell line
View SamplesDectin1 controls the recruitment of TLR9 to -1,3 glucan beads containing phagosomes. We sought to determine whether Dectin-1 also plays a role in controlling TLR9 dependent gene expression.
Dectin-1 Controls TLR9 Trafficking to Phagosomes Containing β-1,3 Glucan.
Specimen part
View SamplesIn high income countries 90% of the patients achieve complete remission after induction chemotherapy. However, 30-40% of these patients suffer from relapse. These patients face a dismal prognosis, as the majority (>60%) of relapsed patients die within 5 years. As a result, outcome for pediatric acute myeloid leukemia (AML) patients remains poor and has stabilized over the past 15 years. To prevent or better treat relapse of AML is the best option to improve outcome. Despite patient specific differences, most patients do respond to initial therapy. This suggests that at relapse, mechanisms are active that cause the altered response to chemotherapy. Detailed understanding of mechanisms that cause relapse remain largely elusive. To gain insight in the molecular pathways that characterize relapsed AML, we performed genome wide gene expression profiling on paired initial diagnosis and relapsed AML samples of 23 pediatric AML patients. We used pathway analysis to find which molecular pathways are involved in altered gene expression between diagnosis and relapse samples of individual AML patients.
Gene expression profiles associated with pediatric relapsed AML.
Disease
View SamplesWe analyzed the transcriptional profile of colon and small-intestinal (SI) tissues in response to ex-vivo colonization with members of the gut microbiota. Tissues were dissected from SPF or GF mice, and connected to the ex-vivo gut organ culture system. Then, microbial cultures or fecal samples were infused into the lumen, and tissues were processed in different time points, as indicated below.
An Intestinal Organ Culture System Uncovers a Role for the Nervous System in Microbe-Immune Crosstalk.
Sex, Age
View SamplesWithin the human gut reside diverse microbes coexisting with the host in a mutually advantageous relationship. We comprehensively identified the modulatory effects of phylogenetically diverse human gut microbes on the murine intestinal transcriptome. Gene-expression profiles were generated from the whole-tissue intestinal RNA of mice colonized with various single microbial strains. The selection of microbe-specific effects, from the transcriptional response, yielded only a small number of transcripts, indicating that symbiotic microbes have only limited effects on the gut transcriptome overall. Moreover, none of these microbe-specific transcripts was uniformly induced by all microbes. Interestingly, these responsive transcripts were induced by some microbes but repressed by others, suggesting different microbes can have diametrically opposed consequences.
Mining the Human Gut Microbiota for Immunomodulatory Organisms.
Sex, Age, Specimen part
View SamplesHere we analyzed the transcriptional profile of S-IECs sorted from GF and monocolonized mice (C. histolyticum and B. adolescentis), as well as SPF mice colonized with SFB or not.
Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice.
Sex, Age
View SamplesWe analyzed the transcriptional profile of small-intestinal lamina propria (SI-LP) CD4+ T cells isolated from germ-free and mice monocolonized with Bifidobacterium adolescentis, SFB, and Nexabiotic (a 23-strain, Th17-inducing, probiotic mix). Overall design: CD4+ T cells were double-sorted from mice directly into lysis buffer.
Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice.
Sex, Age, Specimen part, Cell line, Subject
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