The tumor suppressor p53 induces cellular senescence, an irreversible form of 
proliferation arrest, to inhibit carcinogenesis as well as aging of organs and a 
body. While the major cause of cellular senescence and aging is oxidative 
stress, little is known about how the p53 activity is regulated under such 
conditions. Bach1 inhibits expression of oxidative stress responsive genes by 
competing with Nrf2, the key activator of oxidative stress response. Bach1 
inhibits p53-dependent cellular senescence induced by oxidative stress. Bach1 
forms a protein complex with p53, is recruited to p53 target genes, and inhibits 
their expression. These findings provide completely novel insights into how the 
activity of p53 is regulated under oxidative stress. Since p53 is the critical 
tumor suppressor with huge clinical implications, the newly identified mechanism 
should open new research fields.