title: [Regulation of cellular senescence by Bach1].
abstract: 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.
authors: Department of Biochemistry, Tohoku University Graduate School of Medicine.
authors: Kazuhiko
authors: K
authors: Igarashi
authors: Kazushige
authors: K
authors: Ota
authors: Ayako
authors: A
authors: Nakame
mesh_terms: D000818:Animals; D050976:Basic-Leucine Zipper Transcription Factors / Q000235:genetics*; D016922:Cellular Senescence / Q000502:physiology*; D016158:Genes, p53 / Q000502:physiology; D006801:Humans
chemical_list: C486316:Bach1 protein, mouse; D050976:Basic-Leucine Zipper Transcription Factors