GEO DataSets

Analysis of liver from 4-week old C57BL/6 males with hepatocyte-specific deletion of TGFβ-activated kinase 1 (TAK1). In hepatocytes, TAK1 controls activation of both IKK/NF-κB and JNK pathways. Results provide insight into the role of TAK1 in liver pathophysiology.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL6885

Series:

GSE51962

4 Samples

Download data

(Submitter supplied) The effect of ablation of Tak1 gene in the liver was characterized.

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5474

Platform:

GPL6885

4 Samples

Download data: TXT

(Submitter supplied) Med1 overexpression leads to induction of a wide spectrum of genes. Adenovirally-driven overexpression of Med1 in mouse liver stimulates hepatocyte DNA synthesis with enhanced expression of DNA replication, cell cycle control and liver specific genes as observed at day 3 and day 5 post injection. Med1 gene is amplified in a number of cancers so in this study we tested the hypothesis that Med1 by itself has the capacity to induce cell proliferation. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6887

4 Samples

Download data: TXT

(Submitter supplied) To test whether NDGA attenuate dyslipidemia and hepatic steatosis by enhancing fatty acid oxidation through activation of PPAR-α. Using wild type (WT, C57BL/6) fed with chow diet as control, WT mice were either fed with high-fat diet or high-fat diet with NDGA (2.5g/kg food); ob/ob mice were fed with either chow or chow with NDGA (2.5 g/kg food), and maintained on the respective diets for 16 weeks. The expression of lipid metabolism related genes in the liver of these mice were analyzed using Phalanx GPL6845 platform (Mouse OneArray V1). Together with other biochemical/physiological data, our results suggest that the beneficial actions of NDGA on dyslipidemia and hepatic steatosis in ob/ob mice are exerted primarily through enhanced fatty acid oxidation and energy utilization via the activation of PPAR- α receptor activity.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6845

5 Samples

Download data: GPR

(Submitter supplied) Transforming growth factor beta-activated kinase1 (TAK1) encoded by the gene MAP3K7 regulates multiple important downstream effectors involved in immune response, cell death and carcinogenesis. Hepatocyte-specific deletion of TAK1 in Tak1_Hep mice promotes liver fibrosis and hepatocellular carcinoma (HCC) formation. Here, we report that genetic inactivation of RIPK1 kinase using kinase dead knock-in D138N mutation in Tak1_Hep mice inhibits the expression of liver tumor biomarkers, liver fibrosis and HCC formation. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21273

55 Samples

Download data: CSV, RDATA, TAR, TXT

(Submitter supplied) *Objectives:* In addition to their well-known role in the control of cellular proliferation and cancer, cell cycle regulators are increasingly identified as important metabolic modulators. Genome wide association studies identified SNPs near the cell cycle regulator CDKN2A/p16INK4a (p16) as strongly associated with risk of developing type 2 diabetes (T2D). T2D is associated with numerous perturbations of hepatic lipid and glucose metabolism. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

8 Samples

Download data: CEL

(Submitter supplied) Characterization of chromosomal aberrations in liver tumors of Tak1-/- mice of different ages The aim of the project is to dissect signaling mechanisms which could be of importance during the process of liver carcinogenesis. Keywords: Array comparative genomic hybridization analysis (aCGH).

Organism:

Mus musculus

Type:

Genome variation profiling by array

Platform:

GPL8086

20 Samples

Download data: TXT

(Submitter supplied) Obesity is tightly associated with an increased risk of nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanisms of obesity-induced fatty liver remain largely unknown.In order to identify genes that are potentially involved in dysfunctional hepatic lipid homeostasis in obesity, we performed a clustering analysis of Affymetrix arrays,which revealed that a number of mRNAs were dys-regulated in the livers of mice fed a high-fat diet (HFD), compared with mice fed a normal chow diet (ND).

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) The purpose of this study is to identify the differential transcriptome profiles in WT, hepatic Atg5 KO, TSC1 KO, Atg5/TSC1 DKO, Atg5/TSC1/p62 TKO and Atg5/TSC1/Nrf2 TKO mouse livers. Hepatic mRNA from 2-month-old mice from 5 different mouse strains were extracted and performed for Nextseq analysis in quadruplicates.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21626

24 Samples

Download data: CSV

(Submitter supplied) Purpose: To define the ATF4-dependent transciptional response with feeding in the liver Male mice, 8 weeks of age were subjected to a 12h fast in the light cycle and fed a high carbohydrate diet for 6h in the dark cycle

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

20 Samples

Download data: CSV

(Submitter supplied) Imbalanced mTORC1-S6K1 engages signalling cascades related to obesity and fatty liver. Here, we set up to assess the therapeutic blockage of the ribosomal protein S6 kinase 1 (S6K1) in diet-induced obese (DIO) mice challenged with LY2584702 (LY) tosylate, a specific oral S6K1 inhibitor initially developed for the treatment of solid tumours. To characterize the ability of LY in counteracting obesity and diet-induced disturbances, DIO male mice were challenged every 12 h by oral gavage with LY in treatments lasting 12 and 4 weeks. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL23038

12 Samples

Download data: CEL