TP53 and neoplasm: In contrast, the MAPK p38, which can be activated following inhibition of ERK activity [26] and negatively regulates cell cycle progression at the G1/S and the G2/M transitions by antagonizing the JNK-pathway, down-regulation of cyclins, up-regulation of cyclin-dependent kinase (CDK) inhibitors, and modulation of p53 [27], was phosphorylated and activated to a higher degree in tumor tissue of Bcl-3Hep mice (p < 0.01) compared to the wild type (Figure 3C).