This SuperSeries is composed of the SubSeries listed below.
The role of histone demethylase KDM4B in Myc signaling in neuroblastoma.
Cell line, Treatment
View SamplesEpigenetic alterations appear to modulate Myc signaling. We investigated the role of the histone demethylase JMJD2B in Myc-mediated neuroblastoma pathogenesis. We demonstrate that Myc physically interacts with and recruits this epigenetic modifier, which removes repressive H3K9 methyl marks from Myc-target genes. JMJD2B regulates neuroblastoma proliferation and, together with MYCN amplification, identifies a subgroup of poor prognosis patients. We identify a novel histone demethylase inhibitor, ciclopirox, which targets JMJD2B and, consequently, Myc signaling, thereby inhibiting neuroblastoma proliferation and inducing differentiation. In xenograft studies, genetic and pharmacologic inhibition of JMJD2B resulted in significant tumor growth restriction. Our findings provide insight into epigenetic regulation of Myc via histone methylation and proof-of-concept for pharmacologic inhibition of histone demethylases to target Myc signaling in cancer.
The role of histone demethylase KDM4B in Myc signaling in neuroblastoma.
Cell line, Treatment
View SamplesEpigenetic alterations appear to modulate Myc signaling. We investigated the role of the histone demethylase JMJD2B in Myc-mediated neuroblastoma pathogenesis. We demonstrate that Myc physically interacts with and recruits this epigenetic modifier, which removes repressive H3K9 methyl marks from Myc-target genes. JMJD2B regulates neuroblastoma proliferation and, together with MYCN amplification, identifies a subgroup of poor prognosis patients. We identify a novel histone demethylase inhibitor, ciclopirox, which targets JMJD2B and, consequently, Myc signaling, thereby inhibiting neuroblastoma proliferation and inducing differentiation. In xenograft studies, genetic and pharmacologic inhibition of JMJD2B resulted in significant tumor growth restriction. Our findings provide insight into epigenetic regulation of Myc via histone methylation and proof-of-concept for pharmacologic inhibition of histone demethylases to target Myc signaling in cancer.
The role of histone demethylase KDM4B in Myc signaling in neuroblastoma.
Cell line
View SamplesCord blood stem cells were expanded and differentiated to NK cells. Samples taken at different days after induction of differentiation were analyzed and compared to undifferentiated expanded stem cells. The most highly upregulated genes were further analyzed.
The Transcription Factor ZNF683/HOBIT Regulates Human NK-Cell Development.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The genomic response to retinal disease and injury: evidence for endothelin signaling from photoreceptors to glia.
No sample metadata fields
View SamplesThis experiment was designed to identify transcripts that exhibit changes in abundance in the context of retinal degeneration by comparing transcript levels in adult wild type and prCAD -/- mouse retinas.
The genomic response to retinal disease and injury: evidence for endothelin signaling from photoreceptors to glia.
No sample metadata fields
View SamplesFz2Fz7 double knock out mouse microarray (E8.5)
Frizzled 2 and frizzled 7 function redundantly in convergent extension and closure of the ventricular septum and palate: evidence for a network of interacting genes.
Sex, Specimen part
View SamplesTranscriptional profiles were compared in microdissected lateral walls of the inner ears from Errb mutant mice and wild type littermate controls. The goal is to identify transcriptional targets of Errb and candidate genes for inner ear diseases.
Estrogen-related receptor beta/NR3B2 controls epithelial cell fate and endolymph production by the stria vascularis.
No sample metadata fields
View SamplesTranscriptional profiles were compared between dark adapted and light damaged BALBc (albino) mouse retinas.
The genomic response to retinal disease and injury: evidence for endothelin signaling from photoreceptors to glia.
No sample metadata fields
View SamplesCanonical Wnt signaling in endothelial cells (ECs) is required for vascularization of the central nervous system (CNS) and for formation and maintenance of barrier properties unique to CNS vasculature. Gpr124 is an orphan member of the adhesion G-protein-coupled receptor family that is expressed in ECs and is essential for CNS angiogenesis and barrier formation via an unknown mechanism. Using canonical Wnt signaling assays in cell culture and genetic loss- and gain-of-function experiments in mice, we show that Gpr124 functions as a co-activator of Wnt7a- and Wnt7b-stimulated canonical Wnt signaling via a Frizzled receptor and Lrp co-receptor, and that Gpr124-stimulated signaling functions in concert with Norrin/Frizzled4 signaling to control CNS vascular development. These experiments identify Gpr124 as a ligand-specific co-activator of canonical Wnt signaling. Overall design: Total mRNA from HEK-293/STF cells was subjected to RNAseq
Gpr124 controls CNS angiogenesis and blood-brain barrier integrity by promoting ligand-specific canonical wnt signaling.
No sample metadata fields
View Samples