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Comparision of LPS/GalN-induced gene expression in Rack1F/F and Rack1F/F Alb-cre livers.

ABSTRACT: Comparision of LPS/GalN-induced gene expression in Rack1F/F and Rack1F/F Alb-cre livers.

PROVIDER: PRJNA692736 | ENA |

REPOSITORIES: ENA

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Comparision of LPS/GalN-induced gene expression in Rack1F/F and Rack1F/F;Alb-cre livers.

Project description:In order to further discover the resistance mechanism of Rack1F/F;Alb-cre mice to LPS/ GalN-induced fulfulant hepatitis, we used genome-wide microarray expression profiling as a discovery platform to identify potential genes associated with resistance to LPS/ GalN-induced in Rack1F/F;Alb-cre mice. Fulminant hepatitis was induced by LPS/GalN in Rack1F/F;Alb-cre mice and Rack1F/F mice for 0, 1,3 and 6 hours, respectively.

2021-12-31 | GSE164992 | GEO

Quantitative proteomic analysis of the livers from 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice.

Project description:We have previously shown that the HyD-LIR-Venus probe can specifically inhibit selective autophagy by suppressing the interaction of LIR-containing selective autophagy substrates and receptors with ATG8-family proteins in vivo. We generated hepatocyte-specific HyD-LIR-Venus-expressing mice (HyD-LIRflox/flox; Alb-Cre) by crossing HyD-LIRflox/flox mice, in which HyD-LIR-Venus is expressed under CAG promoter in a Cre-recombinase-dependent manner, with Alb-Cre transgenic mice that express Cre under the control of the Albumin promoter. We performed quantitative proteomic analysis of the livers of 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice using the RTS-SPS-MS3 method on Tribrid mass spectrometry.

2023-04-24 | PXD037013 | JPOST Repository

Hepatic transcriptome analysis of PRDX1fl/fl and Alb-Cre；PRDX1fl/fl mice on MCD

Project description:The etiology of non-alcoholic steatohepatitis (NASH) has been complicated. An increasing body of literature has indicated that hepatic oxidative stress exerts a causal role in driving NASH. Nevertheless, how the anti-oxidant defense system guards against oxidative stress and NASH remains unclear. In this study, we sought to investigate how the peroxidase peroxiredoxin 1 protects against NASH. To this end, we fed WT and hepatic PRDX1 knockout (Alb-Cre;Prdx1fl/fl) a methionine and choline deficient diet (MCD) for 5 weeks and collected liver samples for RNA sequencing analysis. As revealed by gene-set enrichment analysis (GSEA) and KEGG pathway enrichment analysis, there was an enrichment of genes involved in JAK-STAT signaling. Further, we observed that the expression of many genes involved in JAK-STAT signaling such as Pdgfb and Pdgfra was significantly increased in Alb-Cre;Prdx1fl/fl mice. Collectively, these results suggest that increased JAK-STAT signaling accounts for the deteriorated NASH phenotypes in Alb-Cre;Prdx1fl/fl mice.

2023-08-14 | GSE201030 | GEO

Murine hepatocellular carcinoma of MCL1-/- transgenic mice and age matched alb cre mice - 12 months old.

2009-12-31 | GSE16580 | GEO

Genome-wide profiling for H2A.Z and genome accessibility using ATACseq in Uhrf1hepKO mouse livers compared to WT livers

Project description:This study was carried out to investigate potential changes in the genome-wide distribution of H2AZ and genome accessibility using ATACseq in livers where Uhrf1 is deleted in hepatocytes (Uhrf1-fl/fl;Alb:Cre) compared to controls (Uhrf1-fl/fl).

2020-07-17 | GSE153090 | GEO

The Alb-R26Met liver cancer mouse model recapitulates molecular features and heterogeneity of hepatocellular carcinoma patients

Project description:We have generated an inside-out genetic mouse model of liver cancer, the Alb-R26Met mice, in which slightly increased levels of the wild-type form of the MET Receptor Tyrosine Kinase (RTK) occurs specifically in the liver following the deletion of a stop cassette by the Cre recombinase. This genetic combination is obtained by crossing the R26stopMet with Alb-Cre mice. The Alb-R26Met mice spontaneously develop liver tumours and model the whole tumorigenic program. These tumours correspond to HCC patients belonging to the proliferative-progenitor subset. Importantly, the Alb-R26Met model recapitulates several features of HCC patients, including the molecular heterogeneity, the temporal heterogeneity of tumour onset, and the resistance to RTK inhibitors used in the clinic for HCC treatment. This unique genetic setting offered us the possibility to compare the transcriptomic profile of Alb-R26Met non-tumoral livers with Alb-R26Met advanced liver tumours. Outcomes offer an overall vision of how gene expression switches during a tumorigenic process modelled by the Alb-R26Met mice. Importantly, as tumorigenesis in the Alb-R26Met genetic setting occurs in an immune-competent context, outcomes offers as well the possibility to explore the profound changes in the immune microenvironment in the liver tumours, by performing deconvolution of RNAseq data.

2025-02-07 | GSE271709 | GEO

Bulk RNA sequencing of livers from Gubra-Amylin NASH diet fed Chrna2fl/fl and Chrna2fl/fl Alb-Cre mice

Project description:Bulk RNA sequencing of livers from Gubra-Amylin NASH diet fed Chrna2fl/fl and Chrna2fl/fl Alb-Cre mice

| PRJNA825497 | ENA

Murine hepatocellular carcinoma of MCL1-/- transgenic mice and age matched alb cre mice - 12 months old.

Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (12 months) and sex matched alb cre mice. Keywords: Array comparative genomic hybridization analysis (aCGH). Independent HCC of MCL1-/- mice were hybridized with pooled wt mice. Mclâ1flox/flox mice (C57BL/6 background) were obtained from the Dana Farber Cancer Institute, Boston, USA (Opferman JT et al., Nature 2003) and bred to heterozygous Albumin-Cre mice (C57BL/6 background) which led to hepatocyte-specific deletion of Mcl-1. The mice develop severe chronic liver damage (Vick B et al., Hepatology, 2009).

2010-05-16 | E-GEOD-16580 | biostudies-arrayexpress

Genome-wide analysis of livers of control and Lats1/2 deficient neonatal mice [Microarray expression]

Project description:Lats1-/-;Lats2fl/fl;Alb-Cre pups and control pups were sacrificed at 1 day after birth Total mRNA obtained from livers in control and Lats1/2 deficient neonatal mice

2016-06-29 | E-GEOD-71872 | biostudies-arrayexpress

Gene expression profiles in livers with conditional knock out of autophagy related protein 7 (Atg7)

Project description:Expression array analysis of mice livers with conditional deletion of autophagy related protein 7 (Atg7). Whole RNA from mice livers of 2 month old control (Atg7 FF), Olig1-CRE:Atg7 FF (conditional deletion in hepatocytes) and Alb-CRE:Atg7 FF (conditional deletion in hepatocytes/cholangiocytes) were analyzed. The results provide insight into the gene expression profile and role of autophagy in hepatocytes or hepatocytes/cholangiocytes in hepatic growth regulation and hepatocarcinogenesis.

2016-12-31 | GSE67676 | GEO

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