This SuperSeries is composed of the SubSeries listed below.
Addiction of t(8;21) and inv(16) acute myeloid leukemia to native RUNX1.
Cell line
View SamplesCancer cells maintain a sensitive balance between growth-promoting oncogenes and apoptosis inhibitors. We show that WT RUNX1 is required for survival of t(8;21)-Kasumi-1 and inv(16)-ME-1 AML cell lines. The malignant AML phenotype is sustained by a delicate AML1-ETO/RUNX1 balance that involves competition for common DNA binding sites regulating a subset of AML1-ETO/RUNX1 targets.
Addiction of t(8;21) and inv(16) acute myeloid leukemia to native RUNX1.
Cell line
View SamplesTo gain insight into the role of Runx3 in TrkC neurons we performed RNA-seq on E11.5 TrkC neurons isolated from cervical ganglia of Runx3-P2+/- and Runx3-P2-/- mice Overall design: Runx3-P2 mice express GFP in TrkC neurons enabling the FACS isolation of TrkC neurons from E11.5 embryos, Heterozygote Runx3-P2+/-(n=pool of 4) and homozygote Runx3-P2-/- (n=pool of 4) TrkC/GFP neurons were isolated,
An ensemble of regulatory elements controls Runx3 spatiotemporal expression in subsets of dorsal root ganglia proprioceptive neurons.
Specimen part, Cell line, Subject
View SamplesSummary:
HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism.
No sample metadata fields
View SamplesHEK293 cells were transfected with control plasmid (pcDNAI/Neo;Invitrogen) or with the plasmid encoding HCaRG. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen).
HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism.
No sample metadata fields
View SamplesThe histone H3 lysine 9 (H3K9) methyltransferase Eset is an epigenetic regulator critical for the development of the inner cell mass (ICM). Although ICM-derived embryonic stem (ES) cells are normally unable to contribute to the trophectoderm (TE) in blastocysts, we find that depletion of Eset by shRNAs leads to differentiation with the formation of trophoblast-like cells and induction of trophoblast-associated gene expression. Using ChIP-seq analyses, we identified Eset target genes with Eset-dependent H3K9 trimethylation. We confirmed that genes that are preferentially expressed in the TE (Tcfap2a and Cdx2) are bound and repressed by Eset. Single cell PCR analysis shows that the expression of Cdx2 and Tcfap2a is also induced in Eset-depleted morula cells. Importantly, Eset-depleted cells can incorporate into the TE of a blastocyst and subsequently placental tissues. Co-immunoprecipitation and ChIP assays further demonstrates that Eset interacts with Oct4, which in turn recruits Eset to silence these trophoblast-associated genes. Our result suggests that Eset restricts the extraembryonic trophoblast lineage potential of pluripotent cells and links an epigenetic regulator to key cell fate decision through a pluripotency factor.
Eset partners with Oct4 to restrict extraembryonic trophoblast lineage potential in embryonic stem cells.
Specimen part
View SamplesWe used microarrays to detail the global gene expression profiles of OSKM and N2OSKM-infected MEFs over a time course (3, 7, 11 dpi).
The nuclear receptor Nr5a2 can replace Oct4 in the reprogramming of murine somatic cells to pluripotent cells.
Specimen part
View SamplesWe used microarrays to detail the global programme of gene expression of ESCs, Nr5a2 reprogrammed iPSC lines and MEFs.
The nuclear receptor Nr5a2 can replace Oct4 in the reprogramming of murine somatic cells to pluripotent cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The nuclear receptor Nr5a2 can replace Oct4 in the reprogramming of murine somatic cells to pluripotent cells.
Specimen part
View SamplesElectrochemical gradients of monovalent cations across the plasma membrane (high intracellular potassium, [K+]i vs low intracellular sodium, [Na+]i) are created by the Na+,K+-pump and determine a large variety of physiologically important processes. We hypothesized that transcriptomics changes triggered by hypoxia are at least partially caused by Na+i/K+i-mediated excitation-transcription coupling .
Transcriptomic changes triggered by hypoxia: evidence for HIF-1α-independent, [Na+]i/[K+]i-mediated, excitation-transcription coupling.
Specimen part
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