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Analysis of RNA from primary hepatocytes from hepatocyte-specific SRSF1 knockout mice vs. WT

ABSTRACT: RNA from primary hepatocyte cultures from three 3-month-old SRSF1HKO mice compared to RNA from three 3-month-old WT mice for changes in exon utilization and gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE57020 | GEO | 2015/05/01

SECONDARY ACCESSION(S): PRJNA245221

REPOSITORIES: GEO

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Analysis of RNA from primary hepatocytes from hepatocyte-specific SRSF1 knockout mice vs. WT

Project description:RNA from primary hepatocyte cultures from three 3-month-old SRSF1HKO mice compared to RNA from three 3-month-old WT mice for changes in exon utilization and gene expression. SRSF1 KO vs. WT, three replicates each.

2015-05-01 | E-GEOD-57020 | biostudies-arrayexpress

Analysis of RNA from liver tumors in SRSF3 hepatocyte knockout mice

Project description:RNA from three hepatocellular carcinomas from 24-month-old SRSF3HKO mice compared to RNA from non-tumorous liver from 24-month-old SRSF3HKO mice for changes in exon utilization and gene expression.

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Analysis of RNA from liver tumors in SRSF3 hepatocyte knockout mice

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Analysis of liver RNA from SRSF3 hepatocyte knockout mice versus wild-type littermates

Project description:Livers from three SRSF3HKO mice and 3 wild-tyope littermates were used to analyze changes in exon utilization and gene expression.

2012-12-01 | GSE35686 | GEO

Analysis of liver RNA from SRSF3 hepatocyte knockout mice versus wild-type littermates

Project description:Livers from three SRSF3HKO mice and 3 wild-tyope littermates were used to analyze changes in exon utilization and gene expression. two genotypes, three replicates each

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Minimal expression of dysferlin prevents development of muscular dystrophy in dysferlin exon 40a knockout mice

Project description:Dysferlin is an essential muscle membrane repair protein and autosomal recessive mutations in its gene result in progressive muscular dystrophies collectively called dysferlinopathies. We previously showed that calpain-mediated cleavage within dysferlin exon 40a releases a 72kDa C-terminal minidysferlin recruited to injured sarcolemma. In the current study, we hypothesised that knocking out exon 40a will lead to defective membrane repair and development of muscular dystrophy over time. To address this hypothesis, we created three exon 40a knockout (40aKO) mouse lines with dysferlin protein levels ranging from ~80% of wildtype (WT) in 40aKO-3, ~50% in 40aKO-2 and ~10-20% in 40aKO-1 mice. Histopathological analysis of skeletal muscles harvested from all 12-month-old 40aKO mice showed little evidence of dystrophic features seen in dysferlin-null BLAJ mice. Lipidomics analysis on 18wk old quadriceps showed that all 40aKO lines had a similar lipidomic profile to WT and distinct from BLAJs. The proteomic profile of 40aKO lines was intermediate between that of WT and BLAJs. Laser membrane damage assays showed normal membrane repair capacity in all three 40aKO lines. These results collectively indicate that ~10-20% of dysferlin protein expression is sufficient for maintenance of the lipidome and membrane repair capacity, and crucially prevents development of muscular dystrophy.

2023-03-11 | PXD035393 | Pride

Minimal expression of dysferlin prevents development of muscular dystrophy in dysferlin exon 40a knockout mice (second dataset)

2023-03-11 | PXD035918 | Pride

Gene expression profiling of normal mouse hepatocyte, premalignant hepatocytes and fully malignant HCC

Project description:Gene expression was analyzed and compared of normal mouse hepatocyte, premalignant hepatocytes and fully malignant HCC cells. The results provide valuable information about the gene expression alterations during the chronic process of liver cancer development. HCC in age-matched male mice were induced by DEN injection. Normal mouse hepatocyte, premalignant hepatocytes and fully malignant HCC were freshly isolated and RNA extracted.

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Loss of canonical splicing factor SRSF1 in hepatocytes results in acute liver injury and regeneration

Project description:Post-transcriptional gene regulatory mechanisms (PTGRM) contribute profoundly to liver development and physiology. Alternative splicing is one of the earliest mechanisms of gene regulation acting on nascently transcribed mRNA. This process is mediated by a large class of proteins known as splicing factors. SRSF1 is a canonical splicing factor with roles in both constitutive and alternative splicing. While its biochemical activities have been studied extensively, its role in tissue physiology are not well defined. In this study we investigate the role of SRSF1 in liver physiology using hepatocyte-specific knock-out mice models. Hepatocyte-specific knock-out of SRSF1 was achieved in two ways; 1) SRSF1 floxed mice were crossed with AlbCre transgenic mice and 2) SRSF1 floxed mice were injected with AAV8-TBG-iCre viral vector. The latter model allowed for investigating acute changes in hepatocyte upon ablation of SRSF1. Both models exhibit acute liver injury with severe cellular damage, inflammation and lipid accumulation. Utilizing high-throughput transcriptome profiling on purified hepatocytes, we find acute loss of SRSF1 triggers activation of the p53 pathway and splicing dysregulation of genes involved in mRNA metabolism. Continuous hepatic injury in this model eventually triggers a regenerative response resulting in the upregulation of genes involved in proliferation and repopulation of the tissue parenchyma.

2021-03-31 | GSE147005 | GEO

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