Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA122703 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series:; GSE16691: Transcriptional regulation by Norrin-Frizzled4 signaling in the embryonic yolk sac; GSE16703: Long-term effect on the transcriptome of a decrement in Norrin/Frizzled4/Lrp signaling in retinal endothelial cells; GSE16705: Transcriptional response to Frizzled4 signaling in cultured retinal endothelial cells; GSE16707: Long-term effect on the transcriptome of loss of Frizzled4 signaling in cerebellar endothelial cells Experiment Overall Design: Refer to individual Series
2009-10-10 | E-GEOD-16841 | biostudies-arrayexpress
Project description:Transcriptional profiles of the embryonic yolk sac from embryos with ectopic Norrin expression were compared to their wild type littermate controls. The goal is to identify the transcriptional response to Norrin-Frizzled 4 signaling during embryonic angiogenesis. Experiment Overall Design: Ectopic Norrin expression was achieved using a conditional over-expression strategy. Yolk sacs from 3-5 embryos were pooled for each sample and 3 replicates of both control and experimental groups were analyzed.
2009-10-10 | E-GEOD-16691 | biostudies-arrayexpress
Project description:Transcriptional profiles of the embryonic yolk sac from embryos with ectopic Norrin expression were compared to their wild type littermate controls. The goal is to identify the transcriptional response to Norrin-Frizzled 4 signaling during embryonic angiogenesis.
2009-10-01 | GSE16691 | GEO
Project description:Frizzled4 (FZD4) is a pivotal receptor for Norrin and Wnt7a/b that mediates CNS angiogenesis, blood-brain barrier function and blood-retina barrier function. FZD4 is a target for pharmacological interventions in retinal and neurological disease. In order to understand mechanisms of regulation of Frizzled4 activity, two proximity biotinylation screens were performed, one in HEK293T cells and one in HeLa cells. For the screen in HEK293T cells, cells were transiently transfected. 24 hours later, cells were stimulated with 50 µM biotin for an additional 24 hours. Samples were processed and subjected to LC-MS/MSas described (PMID: 29516480). Samples S480 and S483 were biological replicates of cells co-transfected with V5-FZD4-BioID, HA-LRP5, and HA-TSPAN12 to reconstitute the norrin receptor complex. Samples S481 and S484 were biological replicates of cells co-transfected with V5-FZD4-BioID, HA-LRP5, and HA-TSPAN12 that were stimulated with flag-AP-Norrin conditioned media during the 24 hour biotin incubation period to induce norrin/frizzled4 signaling. Sample S479 and S482 were biological replicates of cells co-transfected with GFP-BioID, HA-LRP5, and HA-TSPAN12 as negative control. For the screen in HeLa cells, cells were transfected and biotinylated as described above. Sample S454 was transfected with V5-FZD4 (without BioID fusion, as a negative control). Sample S455 was transfected with GFP-BioID as another negative control. Sample S456 and S457 were transfected with V5-FZD4-BioID, of which only S457 was stimulated with flag-AP-Norrin conditioned medium during the biotin incubation period in order to induce FZD4 endocytosis. Multiple known and novel proximity interactors were identified in HEK293T and HeLa cells with high specificity. Comparisons of cells stimulated with norrin vs. vehicle indicate that proximity interactors of FZD4 were largely similar in cells with and without norrin stimulation in an overexpression context.
2026-05-15 | PXD065058 | Pride
Project description:Using mice with targeted gene mutations, we identify (1) distinct roles for different canonical Wnt signaling components in central nervous system (CNS) vascular development and in the specification of the blood-brain and blood-retina barriers (BBB and BRB) and (2) differential sensitivities of the vasculature in various CNS regions to perturbations in canonical Wnt signaling components. We find nearly equivalent roles for Lrp5 and Lrp6 in brain vascular development and barrier maintenance but a dominant role for Lrp5 in the retinal vasculature, an especially high sensitivity of the BBB in the cerebellum and pons/interpeduncular nuclei to decrements in canonical Wnt signaling, and plasticity in the barrier properties of mature CNS vasculature. Brain and retinal vascular defects caused by loss of Norrin/Frizzled4 signaling can be fully rescued by stabilizing beta-catenin, and loss of beta-catenin’s transcriptional activation domain or expression of a dominant negative Tcf4 recapitulates the vascular development and barrier defects seen with loss of receptor, co-receptor, or ligand, indicating that Norrin/Frizzled4 signaling acts predominantly by beta-catenin-dependent transcriptional regulation. This work strongly supports a model in which identical or nearly identical canonical Wnt signaling mechanisms mediate neural tube and retinal vascularization and maintain the BBB and BRB. Total retina RNA from P10 WT, NdpKO, Ctnnb1flex3/+;Pdgfb-CreER, and NdpKO;Ctnnb1flex3/+;Pdgfb-CreER mice was subjected to RNAseq
2014-06-05 | E-GEOD-56461 | biostudies-arrayexpress
Project description:The transcriptional response to Norrin/Fz4 signaling
| PRJNA243364 | ENA
Project description:KLF2-Regulated Gene Expression in Mouse Embryonic Yolk Sac Erythroid Cells
| PRJNA138277 | ENA
Project description:Using mice with targeted gene mutations, we identify (1) distinct roles for different canonical Wnt signaling components in central nervous system (CNS) vascular development and in the specification of the blood-brain and blood-retina barriers (BBB and BRB) and (2) differential sensitivities of the vasculature in various CNS regions to perturbations in canonical Wnt signaling components. We find nearly equivalent roles for Lrp5 and Lrp6 in brain vascular development and barrier maintenance but a dominant role for Lrp5 in the retinal vasculature, an especially high sensitivity of the BBB in the cerebellum and pons/interpeduncular nuclei to decrements in canonical Wnt signaling, and plasticity in the barrier properties of mature CNS vasculature. Brain and retinal vascular defects caused by loss of Norrin/Frizzled4 signaling can be fully rescued by stabilizing beta-catenin, and loss of beta-catenin’s transcriptional activation domain or expression of a dominant negative Tcf4 recapitulates the vascular development and barrier defects seen with loss of receptor, co-receptor, or ligand, indicating that Norrin/Frizzled4 signaling acts predominantly by beta-catenin-dependent transcriptional regulation. This work strongly supports a model in which identical or nearly identical canonical Wnt signaling mechanisms mediate neural tube and retinal vascularization and maintain the BBB and BRB.
2014-06-05 | GSE56461 | GEO
Project description:Transcriptional response to Frizzled4 signaling in cultured retinal endothelial cells
| PRJNA122805 | ENA