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Status |
Public on Jul 05, 2024 |
Title |
KMT2D regulates gene expression through regulating promoters/enhances upon glucose deprivation. |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing Genome binding/occupancy profiling by high throughput sequencing Other
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Summary |
This SuperSeries is composed of the SubSeries listed below.
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Overall design |
Refer to individual Series
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Citation(s) |
- Liu W, Cao H, Wang J, Elmusrati A et al. Histone-methyltransferase KMT2D deficiency impairs the Fanconi anemia/BRCA pathway upon glycolytic inhibition in squamous cell carcinoma. Nat Commun 2024 Aug 8;15(1):6755. PMID: 39117659
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Submission date |
Jun 12, 2023 |
Last update date |
Aug 30, 2024 |
Contact name |
Cunyu Wang |
E-mail(s) |
cwang@dentistry.ucla.edu
|
Phone |
3108256317
|
Organization name |
UCLA
|
Department |
School of Dentistry
|
Lab |
CHS 56-200
|
Street address |
10833 Le Conte Ave
|
City |
Los Angeles |
State/province |
CA |
ZIP/Postal code |
90095 |
Country |
USA |
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Platforms (2) |
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Samples (29)
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This SuperSeries is composed of the following SubSeries: |
GSE234640 |
KMT2D regulates Fanconi anemia pathway genes through regulating promoters/enhances upon glucose deprivation (CHIPseq) |
GSE234824 |
Whole exome sequencing of HNSCC PDX with KMT2D-inactivating mutation |
GSE237454 |
Gene regulation profiling by KMT2D under different glucose conditions in HNSCC (RNAseq) |
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Relations |
BioProject |
PRJNA982804 |