Regulation of cellular senescence by Bach1

Kazuhiko Igarashi, Kazushige Ota, Ayako Nakame

Research output: Contribution to journalReview articlepeer-review

5 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1423-1428
Number of pages6
JournalNippon rinsho. Japanese journal of clinical medicine
Issue number7
Publication statusPublished - 2009 Jul


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