scispace - formally typeset
Journal ArticleDOI

The codon 72 polymorphic variants of p53 have markedly different apoptotic potential.

Reads0
Chats0
TLDR
It is found that in cell lines containing inducible versions of alleles encoding the Pro72 and Arg72 variants, and in cells with endogenous p53, the Arg72 variant induces apoptosis markedly better than does the Pro 72 variant.
Abstract
The gene TP53, encoding p53, has a common sequence polymorphism that results in either proline or arginine at amino-acid position 72. This polymorphism occurs in the proline-rich domain of p53, which is necessary for the protein to fully induce apoptosis. We found that in cell lines containing inducible versions of alleles encoding the Pro72 and Arg72 variants, and in cells with endogenous p53, the Arg72 variant induces apoptosis markedly better than does the Pro72 variant. Our data indicate that at least one source of this enhanced apoptotic potential is the greater ability of the Arg72 variant to localize to the mitochondria; this localization is accompanied by release of cytochrome c into the cytosol. These data indicate that the two polymorphic variants of p53 are functionally distinct, and these differences may influence cancer risk or treatment.

read more

Citations
More filters
Journal ArticleDOI

Lack of correlation between p53-dependent transcriptional activity and the ability to induce apoptosis among 179 mutant p53s.

TL;DR: It is suggested that transactivation-dependent apoptosis does not always play a major role in p53- dependent apoptosis, indirectly supporting the importance role of the trans activation-independent mechanism.
Journal Article

Retention of the p53 codon 72 arginine allele is associated with a reduction of disease-free and overall survival in arginine/proline heterozygous breast cancer patients.

TL;DR: It is found that the retention of the p53 codon 72 arginine allele in the tumor tissue of proline/arginine heterozygous breast cancer patients is associated with statistically significant reduced disease-free and overall survivals.
Journal ArticleDOI

MDM4 (MDMX) localizes at the mitochondria and facilitates the p53-mediated intrinsic-apoptotic pathway

TL;DR: It is shown that MDM4 stably localizes at the mitochondria, in which it facilitates mitochondrial localization of p53 phosphorylated at Ser46 (p53Ser46P) and promotes binding between p53Ser 46P and BCL2, release of cytochrome C and apoptosis.
Journal ArticleDOI

Mitochondrially Targeted p53 Has Tumor Suppressor Activities In vivo

TL;DR: In vivo data on the direct mitochondrial apoptotic p53 program lays the groundwork to further investigate its efficacy and safety and to address its possible therapeutic value in the future.
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

Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control

TL;DR: The results establish the role of p21CIP1/WAF1 in the G1 checkpoint, but suggest that the anti-apoptotic and theAnti-oncogenic effects of p53 are more complex.
Journal ArticleDOI

Protein regulation by monoubiquitin

TL;DR: Multi-ubiquitin chains at least four subunits long are required for efficient recognition and degradation of ubiquitylated proteins by the proteasome, but other functions of ubiquitin have been discovered that do not involve the protease.
Journal ArticleDOI

Role of a p53 polymorphism in the development of human papillomavirus-associated cancer.

TL;DR: Allelic analysis of patients with HPV-associated tumours revealed a striking overrepresentation of homozygous arginine-72 p53 compared with the normal population, which indicated that individuals homozygously for arginin 72 are about seven times more susceptible to HPV- associated tumorigenesis than heterozygotes.
Journal ArticleDOI

Death signal-induced localization of p53 protein to mitochondria. A potential role in apoptotic signaling

TL;DR: This work proposes a model where p53 can contribute to apoptosis by direct signaling at the mitochondria, thereby amplifying the transcription-dependent apoptosis of p53.
Related Papers (5)