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RNA-sequencing of FACS-sorted Prominin1+ radial glial cells of E12.5 SmadNes mutant embryos (Smad1wt/fl Smad5wt/fl Nestin:Cre+/0) and control littermates (Smad1wt/fl Smad5wt/fl Nestin:Cre0/0)

ABSTRACT: RNA-sequencing of FACS-sorted Prominin1+ radial glial cells of E12.5 SmadNes mutant embryos (Smad1wt/fl Smad5wt/fl Nestin:Cre+/0) and control littermates (Smad1wt/fl Smad5wt/fl Nestin:Cre0/0)

PROVIDER: PRJNA643971 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12143410_1.fastq.gz	Fastqsanger.gz
	SRR12143410_2.fastq.gz	Fastqsanger.gz
	SRR12143411_1.fastq.gz	Fastqsanger.gz
	SRR12143411_2.fastq.gz	Fastqsanger.gz
	SRR12143412_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing of FACS-sorted Prominin1+ radial glial cells of E12.5 SmadNes mutant embryos (Smad1wt/fl;Smad5wt/fl;Nestin:Cre+/0) and control littermates (Smad1wt/fl;Smad5wt/fl;Nestin:Cre0/0)

Project description:We report the transcriptomes of mouse E12.5 cortical radial glial cells and the changes caused by inhibition of the canonical BMP signalling effectors SMAD1/5, whose expression levels are reduced by 50% in the SmadNes mutants.

2020-07-04 | GSE153751 | GEO

Establishment of novel atopic dermatitis model by Nestin-cre mediated Ikk2 deficiency

Project description:To generate novel atopic dermatitis model, we used Nestin-cre mediated Ikk2FL/FL mice. Nestincre-mediated conditional knockout mice of Ikk2 gene were generated by crossing female Ikk2FL/FL mice to male Nestin-cre;Ikk2FL/+mice. Nestin-cre;Ikk2FL/FL mice spontaneously develop chronic AD-like skin inflammation and severe pruritus. We further performed Cap analysis of gene expression (CAGE) to elucidate transcriptional profiles in lesional skin of Nestin-cre;Ikk2FL/FL mice.

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Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi, p53 fl/fl vs Rest GTi/GTi, p53 fl/fl littermates

Project description:We use mice containing a gene trap in the first intron of the Rest gene, which effectively eliminates transcription from all coding exons, to prematurely remove REST from neural progenitors. We find catastrophic DNA damage that occurs during S-phase of the cell cycle, with consequences including abnormal chromosome separation, apoptosis, and smaller brains. Further support for persistent effects is the latent appearance of proneural glioblastomas in adult mice also lacking the tumor suppressor, p53. A Rest deficient mouse line generated previously, using a conventional gene targeting approach, does not exhibit these phenotypes, likely due to a remaining C terminal peptide that still binds chromatin and recruits REST chromatin modifiers.Our results indicate that REST-mediated chromatin remodeling is required for proper S-phase dynamics, prior to its well-established role in relieving repression of neuronal genes at terminal differentiation.

2015-08-01 | GSE68368 | GEO

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi, p53 fl/fl vs Rest GTi/GTi, p53 fl/fl littermates

2015-08-01 | E-GEOD-68368 | biostudies-arrayexpress

Comparison between Nestin+ and Nestin- Ptch1 deficient GNPs

Project description:The intermediate filament protein Nestin serves as a biomarker for stem cells and has been used to identify subsets of cancer stem-like cells. However, the mechanistic contributions of Nestin to cancer pathogenesis are not understood. Here we report that Nestin binds the hedgehog pathway transcription factor Gli3 to mediate the development of medulloblastomas of the hedgehog subtype. In a mouse model system, Nestin levels increased progressively during medulloblastoma formation resulting in enhanced tumor growth. Conversely, loss of Nestin dramatically inhibited proliferation and promoted differentiation. Mechanistic investigations revealed that the tumor-promoting effects of Nestin were mediated by binding to Gli3, a zinc finger transcription factor that negatively regulates hedgehog signaling. Nestin binding to Gli3 blocked Gli3 phosphorylation and its subsequent proteolytic processing, thereby abrogating its ability to negatively regulate the hedgehog pathway. Our findings show how Nestin drives hedgehog pathway-driven cancers and uncover in Gli3 a therapeutic target to treat these malignancies.

2016-08-09 | GSE84392 | GEO

Comparison between Nestin+ and Nestin- Ptch1 deficient GNPs

2016-08-09 | E-GEOD-84392 | biostudies-arrayexpress

Undifferentiated mouse embryonic stem cells, differentiated nestin-positive cells and fibroblast feeder layer.

Project description:Embryonic stem (ES) cells and ES cell-derived progeny characterized by nestin expression (including neural progenitors) were studied (three independent experiments). The mouse ES cell line R1 was cultured on a feeder layer of mouse embryonic fibroblasts (FL). ES cells were differentiated into nestin-positive cells for 4+8 days and 4+11 days according to the differentiation protocol by Rolletschek et al. (Mechanisms of Development 105, 93-104, 2001). The study was performed with three independent cell cultures (= triplicates). RNA was prepared from both undifferentiated ES cells and ES cell-derived nestin-positive cells, and from fibroblast feeder cells. Keywords = ES cell Keywords = nestin positive cells Keywords = feeder layer Keywords: other

2005-09-17 | GSE2375 | GEO

Analysis of difference in transcriptome of Th2 cells derived from Gata3(fl/fl) and Klrg1Cre Gata3(fl/fl) mice

Project description:Purpose: To analyze the transcriptome difference of Th2 cells derived from Gata3(fl/fl) and Klrg1Cre Gata3(fl/fl) mice Method: Lung Th2 cells were used from mice chronically challenged with papain (40 µg/20 µl PBS, 6 subsequent papain challenges, day 0, 1, 2, 13, 14, and 15)

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Transcription profiling of mouse undifferentiated embryonic stem cells, differentiated nestin-positive cells and fibroblast feeder layer.

2008-06-12 | E-GEOD-2375 | biostudies-arrayexpress

Transcription profiling of mouse functionally distinct radial glial subsets

Project description:Since the discovery of radial glia as the source of neurons, their heterogeneity in regard to neurogenesis has been described by clonal and time-lapse analysis in vitro. However, the molecular determinants specifying neurogenic radial glia differently from radial glia that mostly self-renew remain ill-defined. Here, we isolated two radial glial subsets that co-exist at mid-neurogenesis in the developing cerebral cortex and their immediate progeny. While one subset generates neurons directly, the other is largely non-neurogenic but also gives rise to Tbr2-positive basal precursors, thereby contributing indirectly to neurogenesis. Isolation of ; these distinct radial glia subtypes allowed determining interesting differences in their transcriptome. These transcriptomes were also strikingly different from the transcriptome of radial glia isolated at the end of neurogenesis. This analysis therefore identifies, for the first time, the lineage origin of basal progenitors and the molecular differences of this lineage in comparison to directly neurogenic and gliogenic radial glia. Experiment Overall Design: Comparison of radial glial subtypes

2008-06-18 | E-GEOD-8034 | biostudies-arrayexpress

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