By using a genetically accurate mouse model, we demonstrate that endogenous expression of oncogenic N-RasG12D and Tet2 haploinsufficiency collaborate to accelerate CMML development in mice. Gene expression was compared across all genotypes (WT, Tet2+/-, NrasG12D/+ and double mutants) in bone marrow-derived hematopoietic stem cells (CD150+CD48-Lin-Sca1+cKit+) using RNA-seq. N-RasG12D and Tet2 haploinsufficiency cooperate to induce both unique and overlapping effects on HSC gene expression programs. Overall design: Gene expression profiling in FACS-sorted SLAM HSCs from 10-12 week old wild type control (n=3), NrasG12D/+ single mutant (n=3), Tet2+/- single mutant (n=3) and NrasG12D/+;Tet2+/- double mutant (n=3) mice.
Oncogenic N-Ras and Tet2 haploinsufficiency collaborate to dysregulate hematopoietic stem and progenitor cells.
Specimen part, Cell line, Subject
View SamplesAnalysis of gene expression in the meristematic zone of Arabidopsis roots overexpressing miR396
MicroRNA miR396 Regulates the Switch between Stem Cells and Transit-Amplifying Cells in Arabidopsis Roots.
Age, Specimen part
View SamplesStrand-specific RNA sequencing was done on a normal and a cancer cell line to examine how isoforms are used differently between these two states. Overall design: One PrEC sample, a normal cell line. One LNCaP sample, a cancer cell line.
Regional activation of the cancer genome by long-range epigenetic remodeling.
Cell line, Subject
View SamplesCapped analysis of gene expression (CAGE) sequencing was done on a normal and a cancer cell line to examine how promoter usage changes between these two states. Overall design: One PrEC sample, a normal cell line. One LNCaP sample, a cancer cell line.
Regional activation of the cancer genome by long-range epigenetic remodeling.
Cell line, Subject
View SamplesExpression data from 4T1 subclones derived from mammary fat pad tumors (MFP), axillary lymph node tumors (AxLN), and axillary lymph node-derived lung metastases (AxLN-LuM). In parallel, expression data, in the same subclones, of tail vein-derived (TV) lung metastases.
Histone deacetylase 11 inhibition promotes breast cancer metastasis from lymph nodes.
No sample metadata fields
View SamplesIn this study we focussed on malignant post-transplant lymphomas.
Gene expression profiling reveals clear differences between EBV-positive and EBV-negative posttransplant lymphoproliferative disorders.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Consolidation of the cancer genome into domains of repressive chromatin by long-range epigenetic silencing (LRES) reduces transcriptional plasticity.
Specimen part, Cell line
View SamplesThis experiment was set up in order to identify the (direct) transcriptional targets of the Ethylene Response Factor 115 (ERF115) transcription factor. Because ERF115 expression occurs in quiescent center (QC) cells and strong effects on the QC cells were observed in ERF115 overexpression plants, root tips were harvested for transcript profiling in order to focus on root meristem and QC specific transcriptional targets.
ERF115 controls root quiescent center cell division and stem cell replenishment.
Age, Specimen part
View SamplesTo identify genomic regions which display concordant gene expression in prostate cancer, we performed expression profiling of normal prostate epithelial cells (PrEC) and the prostate cancer cell line LNCaP.
Consolidation of the cancer genome into domains of repressive chromatin by long-range epigenetic silencing (LRES) reduces transcriptional plasticity.
Specimen part, Cell line
View SamplesGprc5b, a retinoic acid-inducible orphan G proteincoupled receptor, is a member of the group C metabotropic glutamate receptor family. Its function is unknown. However, recent evidence suggests that it binds Frizzled Wnt receptors and may activate noncanonical Wnt signaling pathways. Here we report the discovery of a brain-enriched C-terminal splice variant of Gprc5b, Gprc5b_v2, by cDNA microarray and RT-PCR analyses. The variant appeared to have been downregulated in the brains of learning/memory-deficient p97FE65 null mice. Despite the fact that the mice had been backcrossed with the C57Bl/6J strain for more than ten generations, Gprc5b and other genes surrounding the FE65 locus on mouse chromosome 7 were retained from the 129-derived ES cells used to generate the knockout line. The differential splicing is unlikely due to FE65 function, as originally suspected, as Gprc5b_v2 expression is also downregulated in the brains of 129/Sv substrains in comparison to C57Bl/6J mice. Further characterization revealed the expression of both Gprc5b_v2 and the previously described variant, Gprc5b_v1, in neurons. Interestingly, Gprc5b_v2 mRNA levels increase with neuronal maturation, paralleling the expression of synaptic proteins involved in the regulation of synaptic plasticity. Finally, we report evidence that both Gprc5b_v2 and Gprc5b_v1 regulate neurite outgrowth. These results are consistent with a putative function of Gprc5b in noncanonical Wnt signaling, which play roles in the regulation of neuronal morphology, and the formation and modulation of neuronal circuitry.
A flanking gene problem leads to the discovery of a Gprc5b splice variant predominantly expressed in C57Bl/6J mouse brain and in maturing neurons.
No sample metadata fields
View Samples