p53 pathway

A model for p53-mediated apoptosis A model for p53-mediated apoptosis. This model depicts the involvement of p53 in the extrinsic and intrinsic apoptotic pathways. p53 target genes are shown in red. The convergence of the two pathways through Bid is shown.

Pathway of renal glutamine catabolism during chronic acidosis Pathway of renal glutamine catabolism during chronic acidosis. Increased renal catabolism of glutamine is sustained during chronic acidosis by increased expression of the glutaminase (GA), glutamate dehydrogenase (GDH) and phosphoenolpyruvate carboxykinase (PEPCK) enzymes and the mitochondrial (mito) glutamine, the apical Na+/H+ and the basolateral Na+3HCO3− transporters. The proteins induced during chronic acidosis are indicated by red arrows. Abbreviations: TCA, tricarboxylic acid cycle; Mal, malate; OAA, oxaloacetate.

Fig. 1. The human GLS2 gene contains a p53 DNA consensus binding element in the promoter region. (A) Putative p53 consensus binding elements in the human GLS2 gene predicted by the p53MH program. N, any nucleotide; Pu, purine; Py, pyramidine. (B) p53 binds to the p53 consensus binding element in the human GLS2 promoter region as detected by ChIP assays. The V138/H1299 cells were shifted to 32 °C for 24 h before assays. The p53-binding element in the MDM2 promoter serves as a positive control. DO-1: p53 antibody. (C) p53 activates luciferase activity of a reporter vector containing the p53-binding element in the GLS2 promoter region. The p53-null H1299 and HCT116 p53−/− cells were cotransfected with the luciferase reporter vectors and vectors expressing either wild-type (pRC p53) or mutant p53 protein (pRC 273H) 24 h before measuring luciferase activities. Hu et al PNAS 2010