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Status |
Public on Sep 26, 2022 |
Title |
Enhancing Acsl4 in absence of mTORC2/Rictor drove β-cell dedifferentiation via inhibiting FoxO1 and promoting ROS production |
Organism |
Mus musculus |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
We here identified Acsl4, a new target of mTORC2, could rescue the impaired β cell proliferation, but not deficient insulin secretion induced by loss of Rictor.
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Overall design |
ex vivo overexpression Acsl4 in βRicKO mice
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Contributor(s) |
Cui C, Gu Y |
Citation(s) |
34455055 |
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Submission date |
Sep 25, 2019 |
Last update date |
Dec 30, 2022 |
Contact name |
canqi cui |
E-mail(s) |
[email protected]
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Organization name |
shanghai national reaearch center for endocrine and metabolic diseases
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Street address |
197 Ruijin 2nd Road
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City |
Shanghai |
ZIP/Postal code |
20025 |
Country |
China |
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Platforms (1) |
GPL24247 |
Illumina NovaSeq 6000 (Mus musculus) |
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Samples (6)
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Relations |
BioProject |
PRJNA574153 |
SRA |
SRP223227 |