๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

The p53 pathway

โœ Scribed by Prives, Carol; Hall, Peter A.


Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
326 KB
Volume
187
Category
Article
ISSN
0022-3417

No coin nor oath required. For personal study only.

โœฆ Synopsis


Abnormalities of the p53 tumour suppressor gene are among the most frequent molecular events in human and animal neoplasia. Moreover, p53 is one of the most studied proteins in the whole of contemporary biology, with more than 12 500 papers so far written! In this review the choice has been deliberately made not to be fully comprehensive in the coverage of the huge p53 literature. Rather attention is focused on a small number of recent developments which are reviewed in the context of modern models of p53 function. Progress in the analysis of signalling to p53 including phosphorylation cascades, and interactions with proteins such as mdm2 and ARF are highlighted. The plethora of protein-protein interactions is discussed, as are the strategies for defining downstream targets of p53. Finally, the emerging biology of p53 homologues is considered. The need for bridging the gap between reductionist, biochemical and biophysical studies and biological and genetic analysis is emphasized. Only this will provide the needed framework for utilizing the information in clinical care.


๐Ÿ“œ SIMILAR VOLUMES


The p53 pathway and apoptosis
โœ Timothy F. Burns; Wafik S. El-Deiry ๐Ÿ“‚ Article ๐Ÿ“… 1999 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 208 KB
The p53 pathway and human cancer
โœ T. Soussi ๐Ÿ“‚ Article ๐Ÿ“… 2005 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 62 KB
Bivariate analysis of the p53 pathway to
โœ James W. Jacobberger; R. Michael Sramkoski; Desheng Zhang; Louis A. Zumstein; Le ๐Ÿ“‚ Article ๐Ÿ“… 1999 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 515 KB

Background: Gene therapy of human tumors with adenovirus vectors presents a clinical research challenge and a potential opportunity in cancer therapy. One of the research challenges is that endpoints like tumor reduction, time to recurrence, and survival do not provide information about whether a po

Tumorigenesis in p27/p53- and p18/p53-do
โœ Lorna A. Damo; Paul W. Snyder; David S. Franklin ๐Ÿ“‚ Article ๐Ÿ“… 2005 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 604 KB

Mice lacking both p18 Ink4c and p27 Kip1 develop a tumor spectrum similar to pRb รพ/ร€ mice, and loss of p53 function accelerates tumorigenesis in pRb รพ/ร€ mice. We hypothesized that codeletion of either p18 or p27 in conjunction with p53 deletion will also accelerate tumorigenesis. Mice lacking both p