Transcriptomics,Genomics

Dataset Information

106

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


ABSTRACT: 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. Overall design: All RNA-seq was performed in duplicates, there are four conditions total. Vector NSCs are the control line and have an empty mCherry vector and a scramble shRNA vector. One hit NSCs express mutant-IDH1 and have a scamble shRNA vector. Two-hit NSCs express mutant IDH1 and have p53 knockdown. Three-hit NSCs express mutant-IDH1, P53 knockdown and ATRX knockdown.

INSTRUMENT(S): Illumina HiSeq 2500 (Homo sapiens)

SUBMITTER: Aram S Modrek  

PROVIDER: GSE94853 | GEO | 2017-11-09

SECONDARY ACCESSION(S): PRJNA374790

REPOSITORIES: GEO

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Publications

Low-Grade Astrocytoma Mutations in IDH1, P53, and ATRX Cooperate to Block Differentiation of Human Neural Stem Cells via Repression of SOX2.

Modrek Aram S AS   Golub Danielle D   Khan Themasap T   Bready Devin D   Prado Jod J   Bowman Christopher C   Deng Jingjing J   Zhang Guoan G   Rocha Pedro P PP   Raviram Ramya R   Lazaris Charalampos C   Stafford James M JM   LeRoy Gary G   Kader Michael M   Dhaliwal Joravar J   Bayin N Sumru NS   Frenster Joshua D JD   Serrano Jonathan J   Chiriboga Luis L   Baitalmal Rabaa R   Nanjangud Gouri G   Chi Andrew S AS   Golfinos John G JG   Wang Jing J   Karajannis Matthias A MA   Bonneau Richard A RA   Reinberg Danny D   Tsirigos Aristotelis A   Zagzag David D   Snuderl Matija M   Skok Jane A JA   Neubert Thomas A TA   Placantonakis Dimitris G DG  

Cell reports 20171001 5


Low-grade astrocytomas (LGAs) carry neomorphic mutations in isocitrate dehydrogenase (IDH) concurrently with P53 and ATRX loss. To model LGA formation, we introduced R132H IDH1, P53 shRNA, and ATRX shRNA into human neural stem cells (NSCs). These oncogenic hits blocked NSC differentiation, increased invasiveness in vivo, and led to a DNA methylation and transcriptional profile resembling IDH1 mutant human LGAs. The differentiation block was caused by transcriptional silencing of the transcriptio  ...[more]

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