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Smart-seq for HBs-specific CD8+ T cells sorted from C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice liver

ABSTRACT: Smart-seq for HBs-specific CD8+ T cells sorted from C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice liver

PROVIDER: PRJNA682742 | ENA |

REPOSITORIES: ENA

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RNA-seq for fetus mice liver tissue of C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice.

Project description:To investigate whether HBsAg intrauterine exposure affected the offspring's immune response against HBV and the relevant mechanism, the difference of fetal liver tissue transcriptome between the C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice was analyzed.

2021-12-01 | GSE162717 | GEO

RNA-seq for fetus mice liver tissue of C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice.

Project description:RNA-seq for fetus mice liver tissue of C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice.

| PRJNA682741 | ENA

Smart-seq for HBs-specific CD8+ T cells sorted from C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice liver

Project description:Previous studies have paid more attention to hepatitis B e antigen (HBeAg) intrauterine exposure, however the effect of solely hepatitis B surface antigen (HBsAg) exposure on the immune response of offspring against hepatitis B virus (HBV) is still unclear. In this study, we investigated whether HBsAg intrauterine exposure affected the offspring's immune response against HBV and the relevant mechanism, which is important for the prevention of HBV mother-to-infant transmission.

2021-12-01 | GSE162718 | GEO

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

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

2009-12-31 | GSE16580 | GEO

Brachypodium distachyon strain:Alb-AL2D | cultivar:Alb-AL2D

Project description:Brachypodium distachyon strain:Alb-AL2D | cultivar:Alb-AL2D Genome sequencing

| PRJNA333719 | ENA

Brachypodium distachyon strain:Alb-AL2F | cultivar:Alb-AL2F

Project description:Brachypodium distachyon strain:Alb-AL2F | cultivar:Alb-AL2F Genome sequencing

| PRJNA333721 | ENA

Brachypodium distachyon strain:Alb-AL2E | cultivar:Alb-AL2E

Project description:Brachypodium distachyon strain:Alb-AL2E | cultivar:Alb-AL2E Genome sequencing

| PRJNA333720 | ENA

C57BL/6 mice

Project description:C57BL/6 mice Targeted loci

| PRJNA546446 | ENA

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

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