Similar studies for GEO DataSets (Select 200061100) - GEO DataSets

Select item 2000611001.

Loss of p21 expression enhances DNA damage, cholestasis and hepatocarcinogenesis in the liver

(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

Series

Accession:: GSE61100

ID:: 200061100

Select item 2000596012.

Hematopoietic cells-derived Jnk1 is crucial for chronic inflammation and carcinogenesis in an experimental model of liver injury

(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

Series

Accession:: GSE59601

ID:: 200059601

Select item 2001568383.

NRF2/KEAP1 in hepatocytes controls fibro- and carcinogenesis in chronic liver disease

(Submitter supplied) Background & Aims: Inflammation in chronic liver diseases induces oxidative stress and thus may contribute to progression of liver injury, fibrosis, and carcinogenesis. The KEAP1/NRF2 axis is a major regulator of cellular redox balance. In the present study, we investigated whether the KEAP1/NRF2 system is involved in liver disease progression in human and mice. Methods: The clinical relevance of oxidative stress was investigated in a well-characterized cohort of NAFLD patients (n=63) by liver RNA sequencing and correlated with histological and clinical parameters. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL11533
24 Samples

Download data: CEL

Series

Accession:: GSE156838

ID:: 200156838

Select item 2001404984.

Hepatocytic c-Jun N-terminal kinases (JNK)-1/2 function determines cell fate during carcinogenesis

(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

Series

Accession:: GSE140498

ID:: 200140498

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000331615.

TNFR1 controls apoptosis and chronic liver disease in hepatocyte-specific IKKγ (Nemo) mice.

(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

Series

Accession:: GSE33161

ID:: 200033161

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 53326.

Death receptor knockout effect on NEMO-deficient model of chronic liver disease

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

DataSet

Accession:: GDS5332

ID:: 5332

PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet

Select item 2001211247.

RNA expression data from hepatocytes from WT, NemoLPC-KO, Cxcr6-/- and NemoLPC-KOCxcr6-/- mice

(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

Series

Accession:: GSE121124

ID:: 200121124

Select item 2000145398.

Chronic liver inflammation-induced double strand DNA breaks enhance hepatocarcinogenesis

(Submitter supplied) Surgical resection is the preferred treatment for Hepatocellular carcinoma; however, it induces tumor recurrence. Our objective was to understand the molecular mechanisms linking liver regeneration under chronic-inflammation to tumorigenesis. Mdr2-knockout mice, a model of inflammation-associated cancer, underwent partial-hepatectomy which led to enhanced hepatocarcinogenesis. Yet, liver regeneration in these mice was severely attenuated. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL8321
21 Samples

Download data: CEL

Series

Accession:: GSE14539

ID:: 200014539

PubMed Full text in PMC Similar studies Analyze with GEO2R

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