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Homo sapiens

ABSTRACT: RNA-seq of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

PROVIDER: PRJNA374790 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5259060_1.fastq.gz	Fastqsanger.gz
	SRR5259060_2.fastq.gz	Fastqsanger.gz
	SRR5259061_1.fastq.gz	Fastqsanger.gz
	SRR5259061_2.fastq.gz	Fastqsanger.gz
	SRR5259062_1.fastq.gz	Fastqsanger.gz

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SOX2 promoter 4C-seq of H9-hESC derived human neural stem cells with mutant IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown

Project description:4C-seq was performed to assess genomic contacts with the SOX2 protmoter, human neural stem cells with no oncogenic alterations were compared to those with concurrent IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown.

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H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

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Homo sapiens

Project description:450k methylation array of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

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Project description:SOX2 promoter 4C-seq of H9-hESC derived human neural stem cells with mutant IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown

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IDH1R132H activity in glioma cell lines and tumnor tissue (2HG)

Project description:We developed genetically engineered mice to generate brain tumors with especific genetic lessions. The animals were split in three groups: NRAS, P53 knockdown, IDH1-R132H and ATRX knock down (NPAID); NRAS, P53 knockdown, IDH1-R132H (NPI); NRAS, P53 knockdown, (NshP53). From these tumor we obtain and culture tumor cells growth like neurospheres and attached cells.

2015-03-05 | ST000312 | MetabolomicsWorkbench

450k methylation array of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

Project description:Methylation profiling was performed to assess methylation alterations by the addition of serial oncogenic hits (mutant-IDH1, P53 knockdown and ATRX knockdown) in human neural stem cells.

2017-11-09 | GSE94956 | GEO

RNA-seq of H9-hESC derived human neural stem cells with combinations of mutant IDH1-R132H overexpression, P53 shRNA knockdown and/or ATRX shRNA knockdown

Project description:RNA-seq was performed to assess gene expression alterations by the addition of serial oncogenic hits (mutant-IDH1, P53 knockdown and ATRX knockdown) in human neural stem cells.

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Differential gene expression in IDH1-R132H Tumor Neurospheres generated from a mouse model of Low Grade Glioma

Project description:IDH1-R132H is expressed in Low Grade Glioma (LGG) in combination with mutation in ATRX and TP53 genes. IDH1-R132H results in gain of function with production of 2-hydroxygluatrate, that in turn generates a hypermethylatyed phenotype in DNA and histone with consequences in epigenetic regulation of gene expression. Here we will compare the gene expression profile between IDH1-R132H and IDH1 Wt tumor neurospheres.

2019-03-18 | GSE94974 | GEO

Differential gene expression in IDH1-R132H Low Grade Glioma animal brain tumors brain in response to 10 Gy of radiation

Project description:IDH1-R132H is expressed in Low Grade Glioma (LGG) in combination with loss of function mutation in ATRX and TP53 genes. IDH1-R132H results in gain of function with production of 2-hydroxygluatrate, that in turn generates a hypermethylatyed phenotype in DNA and histone with consequences in epigenetic regulation of gene expression. Here we will compare the gene expression profile between IDH1-R132H and IDH1 Wt LLG animal brain tumors in reponse to radiation

2019-03-18 | GSE94975 | GEO

Differential gene expression in IDH1-R132H low grade glioma animal brain tumors brain in response to 20 Gy of radiation

Project description:IDH1-R132H is expressed in Low Grade Glioma (LGG) in combination with loss of function mutation in ATRX and TP53 genes. IDH1-R132H results in gain of function with production of 2-hydroxygluatrate, that in turn generates a hypermethylated phenotype in DNA and histone with consequences in epigenetic regulation of gene expression. Here we will compare the gene expression profile between IDH1-R132H and IDH1 Wt LLG moribund animal brain tumors and identify key genes responsible for the phenotype of this subtype of glioma.

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