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Status |
Public on Oct 01, 2015 |
Title |
Atrx facilitate normal neuronal differentiation |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
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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.
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Overall design |
Examined gene expression profiles of three Atrx-deleted neural stem cells and two control ones cultured in two differentiation conditions.
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Contributor(s) |
Li F, Ying J, Yao J, Zheng H |
Citation missing |
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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
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Phone |
713-745-3226
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Organization name |
M. D. Anderson Cancer Center
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Street address |
1515 Holcombe Blvd
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City |
Houston |
State/province |
Texas |
ZIP/Postal code |
77030 |
Country |
USA |
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Platforms (1) |
GPL9185 |
Illumina Genome Analyzer (Mus musculus) |
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Samples (10)
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Relations |
BioProject |
PRJNA297036 |
SRA |
SRP064195 |