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).
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).
Project description:Microarray analysis of liver tissue from WT SIRT6 and conditional knockout of SIRT6 using albumin-Cre (SIRT6Co/Co ;Alb-Cre) at 2 and 8 months of age RNA was extracted from mouse liver tissue at 2 and 8 months of age. RNA from three pairs of WT SIRT6 and SIRT6Co/Co ;Alb-Cre mice was combined and hybridized to Affymetrix mouse gene 1.0 ST arrays.
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.
Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (18 months) and sex matched C57BL/6 mice. Moreover, 18months old C57BL/6 livers were hybridized with independent 18 months old C57BL/6 livers for control. Keywords: Array comparative genomic hybridization analysis (aCGH).
Project description:Microarray analysis of liver tissue from WT SIRT6 and conditional knockout of SIRT6 using albumin-Cre (SIRT6Co/Co ;Alb-Cre) at 2 and 8 months of age
Project description:FBXL6 is frequently over-expressed in human hepatocellular carcinoma (HCC). However, it is still unknown the underlying mechanisms by which FBXL6 promotes HCC. In this study, we compared ubiquitinated protein profiles among a panel of liver tissue samples (including HCC, adjacent tissues and normal tissues) from Fbxl6LSL-fl/+; Alb-cre mice and Alb-cre mice by proteomics and ubiquitomics analysis. There are many proteins with ubiquitination in FBXL6 overexpressed HCC, suggesting ubiquitination may play a critical role in FBXL6-mediated HCC. A1--- normal tissue 1 A2--- normal tissue 2 B1--- Adjacent tissue 1 B2--- Adjacent tissue 2 C1--- HCC tissue 1 C2--- HCC tissue 2
Project description:Hepatocellular carcinoma (HCC) is the fastest growing cause of cancer-related mortality with limited therapies. While endoplasmic reticulum (ER)-stress and the unfolded protein response (UPR) are implicated in HCC, the involvement of the UPR-transducer activating transcription factor 6 alpha (ATF6α) remains unclear. We generated hepatocyte specific n-ATF6 overexpression transgenic mice via Cre-mediated recombination. At 3 months age, livers from the transgenic mice and their wild type controls were harvested for ATAC-sequencing.
Project description:We found that deleting Pten in Albumin expressing cells results in liver steatosis as early as 1 month of age. The mice develop hyperplasia and tumor phenotypes starting at 7-8 months of age. At 12 months and beyond, all mice develope spontanous liver tumors of mixed lineage phenotypes dihydrocollidine (DDC) shows that the primary effect of AKT2 loss is attenuation of hepatic injury and not inhibition of progenitor cell proliferation in response to injury. Pten is deleted specifically in the liver (Pten loxP/loxP; Alb-Cre+). Liver tissues were analyzed at 3 months (steatosis stage) and 15 months (tumor stage)
