Fig. 4: N-RAS deficiency alters the profile of gene expression induced by experimental liver injury and causes overactivation of the JNK and AKT pathways. | Cell Death & Disease

Fig. 4: N-RAS deficiency alters the profile of gene expression induced by experimental liver injury and causes overactivation of the JNK and AKT pathways.

From: Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis

Fig. 4: N-RAS deficiency alters the profile of gene expression induced by experimental liver injury and causes overactivation of the JNK and AKT pathways.The alternative text for this image may have been generated using AI.

A Ingenuity Pathway Analysis (IPA) was performed in N-RAS+/+ and N-RAS−/− livers, 28 days both after CCl4 (left column) and BDL (right column). In blue color, common genes in both models are highlighted. Gene array analysis was performed in N-RAS+/+ and N-RAS−/− livers, 28 days after CCl4 (B) or BDL (C). Correlation of the fold induction of genes in hepatocytes and liver is shown. Log2 expression values of the individual mice were divided by the mean of the sham-operated mice. Log ratios were saved in a .txt file and analyzed with the Multiple Experiment Viewer. Top up- and downregulated genes are shown (red: upregulated; green: downregulated, n = 3 for each model of liver fibrosis, 2.0 < FC > −2.0). D, E Immunoblotting for pJNK, JNK, pJNK1, JNK1, pJNK2, JNK2, pAKT, and AKT) was performed in liver extracts of N-RAS+/+ and N-RAS−/− livers, 28 days after CCl4 (D) and BDL (E), respectively. GAPDH was used as loading control.

Back to article page