This 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 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 SamplesWe analysed the transcriptional signature in endothelial cells extracted from the bone marrow of mice engrafted with human AML and compared it to the one of mice engrafted with human normal hematopoietic cells Overall design: Immunodeficient mice were transplanted with human AML cells derived from patients, or with normal human hematopoietic cells derived from cord blood. Mice were sacrificed once assessed the bone marrow engraftment, and the bones were processed to isolate endothelial cells using the CD31 marker. RNA was extracted, sequencing libraries were prepared and sequenced.
Increased Vascular Permeability in the Bone Marrow Microenvironment Contributes to Disease Progression and Drug Response in Acute Myeloid Leukemia.
Specimen part, Disease, Subject
View SamplesWe sequenced mRNA from Left Ventricles of Streptozotocin induced Type I diabetic mouse hearts or mock treated controls at 4 weeks post-treatment in order to assess alternative splicing changes. Overall design: Heart mRNA profiles of Control and Diabetic (STZ:T1D) mice were generated by deep sequencing using Illumina HiSeq 1000.
Dysregulation of RBFOX2 Is an Early Event in Cardiac Pathogenesis of Diabetes.
Age, Specimen part, Cell line, Treatment, Subject
View SamplesThe response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h.
A conserved PMK-1/p38 MAPK is required in caenorhabditis elegans tissue-specific immune response to Yersinia pestis infection.
Specimen part
View SamplesTo provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa.
Neuronal GPCR controls innate immunity by regulating noncanonical unfolded protein response genes.
Specimen part
View SamplesTo investigate the role of NKX3.1 in prostate differentiation, we employed transcriptome analysis of mouse seminal vesicle (from 15-month-old Nkx3.1+/+ mice); mouse prostate (from 4-month-old Nkx3.1+/+ and Nkx3.1-/- mice); human prostate cells (RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression); and tissue recombinants (generated from combining engineered mouse epithelial cells (seminal vesicle epithelial cells or prostate epithelial cells from 2-month-old mice) and rat UGS mesenchymal cells). Mouse tissue or human cells were snap frozen for subsequent molecular analysis.
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Disease, Disease stage, Treatment
View SamplesAnalysis of the transcriptome of mouse models of prostate cancer after treatment with rapamycin and PD0325901 combination therapy or standard of care docetaxel. The Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) was used in this study. Two months after tumor induction, mice were randomly assigned to vehicle (Veh) or treatments groups, such as rapamycin and PD0325901 (RAPPD) or docetaxel (Docetaxel). For the treatment groups mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) or docetaxel (10 mg/kg) for 5 days (SHORT) or for 1 month (LONG). At the end of the treatment, mice were euthanized, tumors harvested and snap frozen for subsequent molecular analysis.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Treatment
View Samples