GEO DataSets

Analysis of livers from hepatocyte-specific NF-ĸB essential modulator (NEMO), NEMO-TRIAL, and NEMO-TNFR null males. NEMO deletion in hepatocytes causes spontaneous hepatocyte apoptosis. TNFR1 and TRAIL encode death receptors. Results provide insight into the role of death receptors in liver injury.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 4 genotype/variation sets

Platform:

GPL6246

Series:

GSE33161

11 Samples

Download data: CEL

(Submitter supplied) Death receptor-mediated hepatocyte apoptosis is implicated in a wide range of liver diseases including viral hepatitis, alcoholic hepatitis, ischemia/reperfusion injury, fulminant hepatic failure, cholestatic liver injury and cancer. Deletion of NF-ĸB essential modulator in hepatocytes (NemoΔhepa) causes the spontaneous development of hepatocellular carcinoma preceded by steatohepatitis in mice and thus serves as an excellent model for the progression from chronic hepatitis to liver cancer. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5332

Platform:

GPL6246

11 Samples

Download data: CEL

(Submitter supplied) Chronic liver injury triggers complications such as liver fibrosis and hepatocellular carcinoma (HCC), which are associated with alterations in distinct signaling pathways. Of particular interest is the interaction between mechanisms controlled by IKKγ/NEMO, the regulatory IKK subunit, and Jnk activation for directing cell death and survival. In the present study, we aimed to define the relevance of Jnk in hepatocyte-specific NEMO knockout mice (NEMOΔhepa), a genetic model of chronic inflammatory liver injury. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

15 Samples

Download data: CEL

(Submitter supplied) Overexpression of p21 in NEMOΔhepa animals protects against DNA damage, acceleration of hepatocarcinogenesis and cholestasis. As strengthened by our LPS stimulation experiments, we identified a novel protective role of p21 against DNA damage.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

9 Samples

Download data: CEL

(Submitter supplied) Aberrant biliary hyperproliferation resulting from lack of differentiating signals favoring the maintenance of an immature and proliferative phenotype by biliary epithelial cells are ultimately responsible for ducto/cystogenesis and intrahepatic cholangiocarcinoma (CCA) formation. Mitogen-activated protein kinase (MAPK) signaling is pivotal for CCA-related tumorigenesis. In particular, targeted inhibition of JNK signaling has shown therapeutic potential. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11533

24 Samples

Download data: CEL

(Submitter supplied) 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).

Organism:

Mus musculus

Type:

Genome variation profiling by array

Platform:

GPL8086

12 Samples

Download data: TXT

(Submitter supplied) We investigated the role of CXCR6 in the NEMOLPC-KO mouse model. Genetic deletion of CXCR6 enhanced hepatocyte death, inflammation and fibrosis in NEMOLPC-KO mice. This study aimed at characterizing the transcriptomic changes in hepatocytes from these mice compared to controls.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL20775

11 Samples

Download data: CEL

(Submitter supplied) In this study, we found that kinase-dead IKKα knockin (KAL) mice. develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKKα downregulation and marked pulmonary inflammation.KKα downregulation dysregulates the expression of multiple oncogenes and tumor suppressors in K5+ lung epithelial cells. The mutant macrophages increase inflammatory responses and oxidative stress to promote DNA damage in IKKα-mutant K5+ lung epithelial cells, which further dysregulate the levels of multiple oncogenes, tumor suppressors, and stem cell genes, thereby promoting the IKKαlowK5+p63hi cell transition to tumor cells in L-IkkαKA/KA lungs. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

2 Samples

Download data: CEL, CHP, TXT