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SRX6610153: GSM3983371: OGT-deficient liver tissue [OGT_KO_2]; Mus musculus; RNA-Seq
1 ILLUMINA (Illumina NovaSeq 6000) run: 25.3M spots, 7.6G bases, 2.2Gb downloads

Submitted by: NCBI (GEO)
Study: Genome-wide changes in OGT-deficient mouse liver tissue
show Abstracthide Abstract
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 ß-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. 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.
Sample: OGT-deficient liver tissue [OGT_KO_2]
SAMN12391858 • SRS5174385 • All experiments • All runs
Organism: Mus musculus
Library:
Instrument: Illumina NovaSeq 6000
Strategy: RNA-Seq
Source: TRANSCRIPTOMIC
Selection: cDNA
Layout: PAIRED
Construction protocol: Total RNA was extracted from liver tissue with TRIzol reagent according to the manufacturer's protocol.
Experiment attributes:
GEO Accession: GSM3983371
Links:
Runs: 1 run, 25.3M spots, 7.6G bases, 2.2Gb
Run# of Spots# of BasesSizePublished
SRR985622325,262,0187.6G2.2Gb2019-11-07

ID:
8717907

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