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| Status |
Public on Nov 04, 2019 |
| Title |
Genome-wide changes in OGT-deficient mouse liver tissue |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
Over a billion people suffer from chronic liver diseases worldwide, which often leads to fibrosis and then cirrhosis. Treatments for fibrosis remain experimental, in part because no unifying mechanism has been identified that initiates liver fibrosis. O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) plays a pro-survival role under stress in many tissues. Here we report that OGT protects against hepatocyte necroptosis and initiation of liver fibrosis. Decreased O-GlcNAc levels were seen in patients with alcoholic liver cirrhosis and in mice with ethanol-induced liver injury. Liver-specific O-GlcNAc transferase (OGT) knockout (OGT-LKO) mice progressed to liver fibrosis at 10 weeks of age. OGT-deficient hepatocytes underwent necroptosis. These findings identify OGT as a key suppressor of hepatocyte necroptosis and OGT-LKO mice may serve as an effective spontaneous genetic model of liver fibrosis.
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| Overall design |
Total RNA was harvested from the liver tissue of 5-week-old OGT-deleted mice (n=4) and their control littermates (WT, n=5). Both genders were used for the study. Mice were fasted for 6 h before sacrifice.
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| Contributor(s) |
Zhang B, Nam JH, Chung D, Yang X |
| Citation(s) |
31672932, 34146542 |
| Submission date |
Jul 28, 2019 |
| Last update date |
Jul 20, 2021 |
| Contact name |
Xiaoyong Yang |
| E-mail(s) |
xiaoyong.yang@yale.edu
|
| Organization name |
Yale University
|
| Department |
Comparative Medicine
|
| Street address |
375 Congress Ave
|
| City |
New Haven |
| State/province |
CT |
| ZIP/Postal code |
06520-8016 |
| Country |
USA |
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| Platforms (1) |
| GPL24247 |
Illumina NovaSeq 6000 (Mus musculus) |
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| Samples (9)
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| Relations |
| BioProject |
PRJNA557230 |
| SRA |
SRP216750 |
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