TAp73 induction by nitric oxide: regulation by checkpoint kinase 1 (CHK1) and protection against apoptosis.

Nitric oxide (NO) is a potent activator of the p53 tumor suppressor protein, thereby inducing cell cycle arrest and apoptosis. However, little is known about the regulation of the two other p53-family members, p63 and p73, by nitrogen oxides. We report here an up-regulation of p73 by NO in p53-null K-562 leukemia cells.

Glutathione depletion reveals impairment of antigen processing and inhibition of cathepsin activity by nitric oxide in antigen-presenting cells.

Nitric oxide has been shown to induce immunosuppression by inhibiting class II MHC molecule expression and T-lymphocyte proliferation. However, much less is known about the ability of NO to interfere with antigen processing and presentation. So we questioned whether B lymphoma cells exposed to NO could be impaired in their ability to process lysozyme and to stimulate proliferation of a syngeneic T-cell hybridoma.

Upregulation of the p53R2 ribonucleotide reductase subunit by nitric oxide.

The p53R2 ribonucleotide reductase subunit is a p53-inducible protein involved in DNA repair and mitochondrial DNA replication. It has been shown that p53 is activated by nitric oxide, which can damage DNA at high concentrations. This suggests that NO may regulate p53R2 expression through p53 activation.