|
Status |
Public on May 05, 2018 |
Title |
RNAseq for Tfam knock under NKX2.5 promoter |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
|
Summary |
Tfam inactivation by Nkx2.5Cre caused embryonic lethal myocardial hypoplasia. Tfam inactivation was accompanied by elevated production of reactive oxygen species (ROS) and reduced cardiomyocyte proliferation. Mosaic embryonic Tfam inactivation confirmed that the block to cardiomyocyte proliferation was cell autonomous. Transcriptional profiling by RNA-seq demonstrated activation of the DNA damage pathway.
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Overall design |
E13.5 TFAM KOx3; E13.5 TFAM CONx3;
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Contributor(s) |
Zhang D, Li Y, Heims-Waldron D, Guo Y, Gu F, Zhou P, Ma Q, Pu WT |
Citation(s) |
29021295 |
|
Submission date |
May 05, 2017 |
Last update date |
Jul 25, 2021 |
Contact name |
Fei Gu |
E-mail(s) |
alickgf@hotmail.com
|
Organization name |
Childrens hospital boston, Harvard Medical School
|
Department |
Cardiology
|
Lab |
William Pu
|
Street address |
320 Longwood Ave.
|
City |
Boston |
State/province |
MA |
ZIP/Postal code |
02115 |
Country |
USA |
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Platforms (1) |
GPL17021 |
Illumina HiSeq 2500 (Mus musculus) |
|
Samples (6)
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Relations |
BioProject |
PRJNA385566 |
SRA |
SRP106520 |