Ontology highlight
ABSTRACT:
PROVIDER: PRJNA803319 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Regulation of embryonic liver growth remains largely elusive. Progranulin has been discussed in pathological liver growth; however, the functional role of Pgrn in embryonic liver growth has never been addressed. Knockdown of GrnA, the orthologue of mammalian pgrn in zebrafish, displayed a deficient hepatic outgrowth during hepatogenesis. Expression profiles manifested that pgrn-deficiency impaired hepatogenesis associated with dysregulation of Met signaling. Pgrn regulates hepatic expression of Met was further verified in vitro and in vivo. These results indicate that Pgrn is a novel factor required for embryonic hepatic outgrowth and reveal a novel link between Pgrn and Met signaling. To explore the GrnA induced genomic responses during hepatic outgrowth, mRNA expression profiles were compared from grnA morphants and control embryos using zebrafish 14K oligonucleotide microarray at 72 hpf, when hepatocytes were rapid proliferating.
2010-11-10 | E-GEOD-19211 | biostudies-arrayexpress
Project description:This project is designed to measure changes in gene expression during sea lamprey development RNA was extracted from sea lamprey embryos at 1, 2, 2.5, 3, 4, and 5 days post-fertilization and used to generate RNAseq data
2016-06-28 | E-GEOD-76037 | biostudies-arrayexpress
Project description:This project is designed to measure changes in gene expression during sea lamprey development and in the adult germline RNA was extracted in biological triplicate from sea lamprey embryos at 1, 2, 2.5, 3, 4, and 5 days post-fertilization and in technical replicates from adult testes using trizol extraction. RNA was analyzed on the Nanostring nCounter gene expression assay to measure changes in gene expression across developmental time points and in adult testes
2016-10-21 | E-GEOD-76064 | biostudies-arrayexpress
Project description:Regulation of embryonic liver growth remains largely elusive. Progranulin has been discussed in pathological liver growth; however, the functional role of Pgrn in embryonic liver growth has never been addressed. Knockdown of GrnA, the orthologue of mammalian pgrn in zebrafish, displayed a deficient hepatic outgrowth during hepatogenesis. Expression profiles manifested that pgrn-deficiency impaired hepatogenesis associated with dysregulation of Met signaling. Pgrn regulates hepatic expression of Met was further verified in vitro and in vivo. These results indicate that Pgrn is a novel factor required for embryonic hepatic outgrowth and reveal a novel link between Pgrn and Met signaling.
2010-11-10 | GSE19211 | GEO
Project description:Progranulin (PGRN) is a lysosomal protein involved in various neurodegenerative diseases. Over 70 mutations discovered in the GRN gene all result in reduced expression of PGRN protein. However, the detailed molecular function of PGRN within lysosomes and the impact of PGRN deficiency on lysosomal biology remain unclear. Here we leveraged multi-faceted proteomic techniques to comprehensively characterize how PGRN deficiency changes the molecular and functional landscape of neuronal lysosomes.
2023-02-18 | MSV000091322 | MassIVE
Project description:Gene expression microarrays were used to identify how the mRNA phenotype of NSC-34 cells responds to PGRN expression levels. PGRN expression correlated well with molecular phenotypes that included mRNA pathways associated with the regulation of the cytoskeleton Gene expression profile was determined using Illumina Mouse Whole-Genome Expression BeadChips (MouseWG-6 v2.0
2021-10-14 | GSE185877 | GEO
Project description:To understand how haploinsufficiency of progranulin (PGRN) protein causes frontotemporal dementia (FTD), we created induced pluripotent stem cells (iPSC) from patients carrying the GRNIVS1+5G>C mutation (FTD-iPSCs). FTD-iPSCs were fated to cortical neurons, the cells most affected in FTD and known to express PGRN. Although generation of neuroprogenitors was unaffected, their further differentiation into neurons, especially CTIP2-, FOXP2- or TBR1-TUJ1 double positive cortical neurons, was significantly decreased in FTD-neural progeny. Zinc finger nuclease-mediated introduction of PGRN cDNA into the AAVS1 locus corrected defects in cortical neurogenesis, demonstrating that PGRN haploinsufficiency causes inefficient cortical neuron generation. RNAseq analysis confirmed reversal of altered gene expression profile following genetic correction. Wnt signaling pathway, one of the top defective pathways in FTD-iPSC-derived neurons coupled with its reversal following genetic correction, makes it an important candidate. Therefore, we demonstrate for the first time that PGRN haploinsufficiency hampers corticogenesis in vitro.
2014-11-12 | GSE60902 | GEO