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Series GSE73447 Query DataSets for GSE73447
Status Public on Oct 01, 2015
Title Atrx facilitate normal neuronal differentiation
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Summary Purpose: the chromatin-remodeler ATRX is frequently mutated in a range of human malignancies including pediatric and adult gliomas, and its loss underlies induction of alternative lengthening of telomeres (ALT) pathway for chromosome-end maintenance. But how ATRX exters its glioma suppresor role remains unclear. Here, we combine RNAi and somatic deletion approaches to demonstrate ATRX as a glioma suppressor controlling neural differentiation. Loss of ATRX promotes gliomagenesis by blocking neuronal progenitors from undergoing terminal maturation. Our findings provide the molecular and cellular mechanism underline ATRX's function in gliomagenesis.
 
Overall design Examined gene expression profiles of three Atrx-deleted neural stem cells and two control ones cultured in two differentiation conditions.
 
Contributor(s) Li F, Ying J, Yao J, Zheng H
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Submission date Sep 25, 2015
Last update date May 15, 2019
Contact name Chunru Lin
E-mail(s) CLin2@mdanderson.org
Phone 713-745-3226
Organization name M. D. Anderson Cancer Center
Street address 1515 Holcombe Blvd
City Houston
State/province Texas
ZIP/Postal code 77030
Country USA
 
Platforms (1)
GPL9185 Illumina Genome Analyzer (Mus musculus)
Samples (10)
GSM1894022 Control NSC#1
GSM1894023 Control NSC#2
GSM1894024 Control NSC#1-differentiation
Relations
BioProject PRJNA297036
SRA SRP064195

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE73447_TPM.HWZheng.RNAseq.150725.txt.gz 561.6 Kb (ftp)(http) TXT
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Raw data are available in SRA
Processed data are available on Series record

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