This 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 SamplesThis study explores the impact of lifestyle and environment on gene expression through whole transcriptome profiling of peripheral blood samples in Fijian population (native Melanesians and Indians) living in the rural and urban areas.
Using blood informative transcripts in geographical genomics: impact of lifestyle on gene expression in fijians.
Sex, Age, Specimen part, Subject
View SamplesFz4 and Fz8 cooperate in regulating the branching morhpogenesis of the developing kidney during mouse embryonic development, hence determines the eventual kidney size.
Genetic mosaic analysis reveals a major role for frizzled 4 and frizzled 8 in controlling ureteric growth in the developing kidney.
Specimen part
View SamplesEndothelin signaling is required for neural crest migration and homeostatic regulation of blood pressure. Here we report that constitutive over-expression of Endothelin-2 (Edn2) in the mouse retina perturbs vascular development by inhibiting endothelial cell (EC) migration across the retinal surface and subsequent EC invasion into the retina. Developing endothelial cells exist in one of two states: tip cells at the growing front, and stalk cells in the vascular plexus behind the front. This division of endothelial cell states is one of the central organizing principle of angiogenesis. In the developing retina, Edn2 over-expression leads to over-production of endothelial tip cells by both morphologic and molecular criteria. Spatially localized over-expression of Edn2 produces a correspondingly localized endothelial response. Edn2 over-expression in the early embryo inhibits vascular development at mid-gestation, but Edn2 over-expression in developing skin and brain has no discernable effect on vascular structure. Inhibition of retinal angiogenesis by Edn2 requires expression of Endothelin receptor A (Ednra) but not Ednrb in the neural retina. Taken together, these observations imply that the neural retina responds to Edn2 by synthesizing one or more factors that promote the endothelial tip cell state and inhibit angiogenesis. The response to Edn2 is sufficiently potent that it over-rides the activities of other homeostatic regulators of angiogenesis, such as vascular endothelial growth factor.
Endothelin-2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis.
Specimen part
View SamplesCockayne syndrome (CS) is an autossomal human disorder characterized by premature aging along with other symptoms. At the molecular level, CS is characterized by a deficiency in the Transcription-couple DNA repair pathway caused by a mutation mainly in ERCC6 gene and the absence of its functional protein. It has been shown that the presence of DNA damage and the lack of some functional proteins related to DNA repair constitute a barrier for somatic cell reprogramming. Recently, it was demonstrated that one protein involved in Genome Global Repair controls the expression of an important pluripotent gene, highligting its importance for cellular reprogramming.
Evidence for premature aging due to oxidative stress in iPSCs from Cockayne syndrome.
Specimen part, Disease, Cell line
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