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Status |
Public on May 06, 2017 |
Title |
RNA-seq analysis of Kdm6a deficient brains in mice |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
Kdm6a is an X-linked histone demethylase that activates gene expression via removal of the repressive methylation mark at histone H3 lysine 27 (H3K27). In humans, KDM6A mutations cause Kabuki syndrome, a disorder characterized by intellectual disability and motor coordination deficits. To assess the role of Kdm6a in brain development and behavior, we generated a neuron-specific Kdm6a deficient mouse model using Cre-LoxP recombination. The mutant mice exhibited an adult-onset deficit in motor coordination. We then performed RNA-seq analysis to determine the mis-regulated genes that are listed in this dataset.
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Overall design |
Genome-wide gene expression was determined in the brain between 3 adult male Kdm6a deficient and 3 wild type littermate mice.
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Contributor(s) |
Xu J, Li R |
Citation missing |
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NIH grant(s) |
Grant ID |
Grant title |
Affiliation |
Name |
R01 MH096066 |
Novel epigenetic mechanisms in neuronal development and cognitive function |
CHILDREN'S HOSPITAL |
XU |
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Submission date |
May 09, 2016 |
Last update date |
May 15, 2019 |
Contact name |
Rui Li |
Organization name |
University of Massachusetts Medical School
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Department |
MCCB
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Street address |
364 Plantation Street, LRB
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City |
Worcester |
State/province |
Massachusetts |
ZIP/Postal code |
01605 |
Country |
USA |
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Platforms (1) |
GPL17021 |
Illumina HiSeq 2500 (Mus musculus) |
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Samples (6)
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Relations |
BioProject |
PRJNA321062 |
SRA |
SRP074611 |