The Two French Lords of “All's Well That Ends Well”

Levin, Richard

doi:10.1093/nq/26-2-122

Cited by 15 publications

(20 citation statements)

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“…The first group of genes encodes proteins that localize to the cell membrane (e.g., CD95, KILLER/DR5, PERP) (Owen-Schaub et al, 1995;Muller et al, 1998;Wu et al, 1997Wu et al, , 1999Attardi et al, 2000). The second group of genes encodes proteins that localize to the cytoplasm, including PIDD and PIGs Lin et al, 2000). The third group of genes encodes proteins that localize to the mitochondria (e.g., BAX, NOXA, PUMA, P53 Aip1 , BID) (Miyashita et al, 1995;Oda et al, 2000a, b;Sax et al, 2002).…”

Section: P53-mediated Apoptosis In Irmentioning

confidence: 99%

P53 and radiation responses

2003

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Cells have evolved elaborate mechanisms (checkpoints) to monitor genomic integrity in order to ensure the highfidelity transmission of genetic information. Cells harboring defects in checkpoint pathways respond to DNA damage improperly, which in turn may enhance the rate of cancer development. Ionizing radiation (IR) primarily leads to double-strand DNA breaks (DSBs), which activate DNA damage checkpoints to initiate signals ultimately leading to a binary decision between cell death and cell survival. TP53 has been recognized as an important checkpoint protein, functioning mainly through transcriptional control of target genes that influence multiple response pathways and leading to the diversity of responses to IR in mammalian cells. We review how the tumor suppressor P53 is involved in the complex response to IR to enforce the cell's fate to live by inducing the growth arrest coupled to DNA damage repair or to die by inducing irreversible growth arrest or apoptosis. Moreover, recent insights have emerged in our understanding of how P53 modulates radiosensitivity in tissues following IR as well as its role in sensitizing cells to chemo-and radiotherapy. The P53 pathway remains an attractive target for exploitation in the war on cancer.

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Section: P53-mediated Apoptosis In Irmentioning

confidence: 99%

P53 and radiation responses

2003

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“…If this is by mediating apoptosis, as is often argued, we must recognize that the mechanism by which p53 mediates apoptosis has become increasingly less clear in recent years as the list of p53-regulated proapoptotic candidates has grown sharply. Included among these are: Bax, CD95/Fas, Noxa, Pidd, PIG3, p53AIP1, PUMA, mtCLIC/CLIC4 and Scotin (Miyashita and Reed, 1995;Owen-Schaub et al, 1995;Polyak et al, 1997;Lin et al, 2000;Oda E et al, 2000;Oda K et al, 2000;Nakano and Vousden, 2001;Yu et al, 2001;Bourdon et al, 2002;Fernandez-Salas et al, 2002). Importantly, we lack data on whether these various proteins are coregulated, and how they might interact.…”

Section: Targeting P53mentioning

confidence: 99%

Strategies for reversing drug resistance

2003

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“…Several of the p53 inducible genes encode proteins that have been implicated in having a potential role in apoptosis. These include the bcl-2 related proapoptotic genes bax (reviewed in Lotem and Sachs, 1999) and Noxa (Oda et al, 2000a), death domain containing genes DR5, FAS (reviewed in Lotem and Sachs, 1999) and Pidd (Lin et al, 2000), the mitochondrial genes p53AIP1 (Oda et al, 2000b) and PUMA (Nakano and Vousden, 2001; Yu et al, 2001), the ced-4 homolog Apaf-1 (Kannan et al, 2001;Moroni et al, 2001) and the genes PERP (Attardi et al, 2000) and p53DINP1 (Okamura et al, 2001). Some of the p53 repressible genes are apoptosis suppressors including bcl-2 (Lotem and Sachs, 1995a), the IGF-1 receptor (Prisco et al, 1997), heat shock protein 70 (HSP70) (Ago et al, 1993) and p202 (D'Souza et al, 2001).…”

Section: Cytokines As Suppressors Of Apoptosismentioning

confidence: 99%