scispace - formally typeset
Open AccessJournal ArticleDOI

A ribonucleotide reductase gene is a transcriptional target of p53 and p73.

Katsunori Nakano, +3 more
- 31 Aug 2000 - 
- Vol. 19, Iss: 37, pp 4283-4289
TLDR
The identification of a close relative of ribonucleotide reductase, recently named p53R2, as a p53-inducible gene, supports a direct role for p53 in DNA repair, in addition to inhibition of growth of damaged cells.
Abstract
Many p53-inducible genes have been identified that might play a role in mediating the various downstream activities of p53. We have identified a close relative of ribonucleotide reductase, recently named p53R2, as a p53-inducible gene, and show that this gene is activated by several stress signals that activate a p53 response, including DNA damaging agents and p14ARF. p53R2 expression was induced by p53 mutants that are defective for the activation of apoptosis, but retain cell cycle arrest function, although no induction of p53R2 was seen in response to p21WAF1/CIP1-mediated cell cycle arrest. Several isoforms of the p53 family member p73 were also shown to induce p53R2 expression. Transient ectopic expression of either wild type p53R2 or p53R2 targeted to the nucleus, did not significantly alter cell cycle progression in unstressed cells. The identification of this gene as a p53 target supports a direct role for p53 in DNA repair, in addition to inhibition of growth of damaged cells.

read more

Citations
More filters
Journal ArticleDOI

Live or let die: the cell's response to p53

TL;DR: Understanding the complex mechanisms that regulate whether or not a cell dies in response to p53 will ultimately contribute to the development of therapeutic strategies to repair the apoptotic p53 response in cancers.
Journal ArticleDOI

PUMA, a novel proapoptotic gene, is induced by p53.

TL;DR: A novel gene named PUMA (p53 upregulated modulator of apoptosis) is identified as a target for activation by p53, and PUMA is likely to play a role in mediating p53-induced cell death through the cytochrome c/Apaf-1-dependent pathway.
Journal ArticleDOI

TIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis

TL;DR: expression of TIGAR may modulate the apoptotic response to p53, allowing survival in the face of mild or transient stress signals that may be reversed or repaired, and the decrease of intracellular ROS levels in response to TIGar may also play a role in the ability of p53 to protect from the accumulation of genomic damage.
Journal ArticleDOI

Regulation and function of the p53 tumor suppressor protein.

TL;DR: The p53 tumor suppressor pathway is a nuclear protein that functions as a regulator of transcription and the mechanisms by which p53 mediates its effects are studied.
Journal ArticleDOI

The Evolution of Iron Chelators for the Treatment of Iron Overload Disease and Cancer

TL;DR: This review focuses on the evolution of iron chelators from initial lead compounds through to the development of novel chelating agents, many of which show great potential to be clinically applied in the treatment of iron overload disease and cancer.
References
More filters
Journal ArticleDOI

WAF1, a potential mediator of p53 tumor suppression

TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
Journal ArticleDOI

Requirement for p53 and p21 to Sustain G2 Arrest After DNA Damage

TL;DR: After DNA damage, many cells appear to enter a sustained arrest in the G2 phase of the cell cycle but this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21.
Journal ArticleDOI

p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development

TL;DR: It is reported that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development, and results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelialDevelopment and morphogenesis.
Journal ArticleDOI

p63 is a p53 homologue required for limb and epidermal morphogenesis.

TL;DR: P63 is essential for several aspects of ectodermal differentiation during embryogenesis, including hair follicles, teeth and mammary glands, which are absent in p63-deficient mice.
Journal Article

p21 is necessary for the p53-mediated G1 arrest in human cancer cells.

TL;DR: Results unambiguously establish p21 as a critical mediator of one well-documented p53 function and have important implications for understanding cell cycle checkpoints and the mechanism(s) through which p53 inhibits human neoplasia.
Related Papers (5)