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Transcriptomic analysis of Pot1a/b knockout in a native mouse model of glioma

ABSTRACT: Transcriptomic analysis of Pot1a/b knockout in a native mouse model of glioma

PROVIDER: PRJNA679565 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13086118_1.fastq.gz	Fastqsanger.gz
	SRR13086118_2.fastq.gz	Fastqsanger.gz
	SRR13086119_1.fastq.gz	Fastqsanger.gz
	SRR13086119_2.fastq.gz	Fastqsanger.gz
	SRR13086120_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of Pot1a/b knockout in a native mouse model of glioma

Project description:Please see the cited publication below for further details. This study found that Pot1a/b knockout in a native mouse model of glioma confers sexual dimorphism of survival and discovered sex-dependent changes in telomere content as well as signatures of immune infiltration and cell cycle in these tumors.

2021-01-31 | GSE161823 | GEO

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Gene Expression Profile of high grade glioma in Ascl1creERTM driven tumor suppressors knockout mouse model

Project description:Mouse model with P53f/f;Nf1f/f or P53f/f; Nf1f/- driven by Ascl1creERTM induced at 1 month postnatally forms high grade glioma in the brain. Tumors were harvested and total RNA were extracted for gene expression profile. Ten tumors were harvested from the Ascl1creERTM mouse model with desired genotype when showing neurological symptomes. Eight control brain tissue were harvested at corresponding anatomaical regions in the control mice. Total RNA were extracted from the tumor tissue and control tissue

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Expression analysis of MADM based glioma mouse model

Project description:Mosaic Analysis with Double Markers (MADM) based glioma mouse model, which homozygously lacks Tp53 and Nf1, spontaneously developed gliomas at the post-natal 90-120 days. Tp53 and Nf1 are among the most frequently mutated genes in human glioma patients. Investigating the expression changes of genes induced by inactivation of Tp53 and Nf1 can be a clue to clarify the mechanism of gliomagenesis. We examined the expressions of glioma in MADM mouse at post-natal 150 days (n=3) and of normal brain in Tp53 and Nf1 wild type mouse at post-natal 150 days (n=2). We used SurePrint G3 Mouse GE 8×60K array slides (G4858A, Agilent Technologies).

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ChIP analysis of MADM based glioma mouse model

Project description:Mosaic Analysis with Double Markers (MADM) based glioma mouse model, which homozygously lacks Tp53 and Nf1, spontaneously developed gliomas at the post-natal 90-120 days. Tp53 and Nf1 are among the most frequently mutated genes in human glioma patients. Investigating the changes of histone modifications induced by inactivation of Tp53 and Nf1 can be a clue to clarify the mechanism of gliomagenesis. We examined the histone modifications of glioma in MADM mouse at post-natal 150 days (n=3) and post-natal 8 days (n=1) and NSC, astrocyte derived from normal mice brain (both n=1) ). We used customized SurePrint G3 Mouse GE 2×400K array slides (G4858A, Agilent Technologies).

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Gene Expression Profile of high grade glioma in Nestin-creERT2 and NG2-creERTM driven tumor suppressors knockout mouse model

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Project description:Mouse model with P53f/f;Nf1f/+;Ptenf/+ configuration driven by Nestin-creERT2 and NG2-creERTM induced at 1 month postnatal forms high grade glioma in the brain. Tumors were harvested and total RNA were extracted for gene expression profile. Three tumors were harvested from the Nestin-creERT2 mouse model and 5 tumors were harvested from the NG2-creERTM mouse model with desired genotype when mice show neurological symptomes. Three control brain tissue for each model were harvested at corresponding anatomical position in the control mice. Total RNA were extracted from the tumor tissue and control tissue

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Project description:As a starting point for dissecting the cellular heterogeneity of gliomas, different subpopulations from a CRISPR mouse model of glioma were profiled for gene expression. Because we initially identified these astrocyte subpopulations in the mouse brain, we first sought to determine whether their malignant analogues are present in mouse models of glioma. Towards this, we recently developed a mouse model of malignant glioma, one that utilizes E16.5 IUE approaches in combination with CRISPR mediated gene editing, where we use IUE to introduce gRNA vectors to delete NFI, PTEN, and p53, CAS9, and a GFP reporter, resulting in the generation of malignant glioma at P70. Using the GFP label to distinguish tumor from normal brain tissue, along with FACS-based selection against the glioma stem cell (GSC) and endothelial cells (see methods), we screened our tumor models for the presence of these prospective astroglial populations in the non-GSC fractions of these tumors.

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2020-02-20 | GSE110927 | GEO

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